VEDOLIZUMAB FOR THE TREATMENT OF PEDIATRIC PATIENTS.

Abstract

The invention provides methods for the treatment of pediatric patients with inflammatory bowel disease using vedolizumab.

Description

METHODS FOR TREATING PEDIATRIC DISORDERS RELATED APPLICATIONS This application claims priority over U.S. provisional application number 562 / 492,031, filed on April 28, 2017. The entire contents of the foregoing application are incorporated herein by reference LIST OF SEQUENCES This application contains a list of sequences that was submitted electronically in ASCII format and is incorporated herein in its entirety by this reference. This ASCII copy, created on April 25, 2018, is named 079259-0839_SLtxt and has a size of 12,557 bytes. BACKGROUND The incidence of pediatric inflammatory bowel disease (IBD) appears to be increasing. According to the Crohn's and Colitis Foundation of America, approximately 1 million Americans have either ulcerative colitis or Crohn's disease, of whom roughly 15 out of 100,000 are under 21 years of age. IBD, like ulcerative colitis and Crohn's disease, for example, can be a debilitating and progressive illness involving inflammation of the gastrointestinal tract. While the symptoms of ulcerative colitis are similar in both pediatric and adult populations, pediatric patients usually present with more extensive disease. For approximately 20–25% of patients with IBD, the onset of the disease occurs during childhood or adolescence. Treatments for IBD have included anti-inflammatory drugs (such as corticosteroids and sulfasalazine), immunosuppressant drugs (such as 6-mercaptopurine, cyclosporine, and azathioprine), and surgery (such as colectomy). Podolsky, New Engl. J. M&d, 325:928-937 (1991) and Podolsky, New Engl. J. Med., 325:1008-1016 (1991). As the disease progresses, treatment advances to regimens that expose the patient to a progressively increasing risk of side effects and a decline in quality of life. Integrin receptors are important for regulating both lymphocyte recirculation and recruitment to sites of inflammation (Carlos, TM, and Harían., JM, Bloed, 84:2068-2101 (1994)). Human integrin α4β7 has several ligands, one of which is the vascular mucosal addressin MAdCAM-1 (Berlin, C., et al., Ce / / 74; 185-195 (1993); Erle, DJ„ et al., J. Immunol 153:517-528 (1994)), which is expressed in upper endothelial venules in mesenteric lymph nodes and Peyer's patches (Sfreeter, PR, et al., Natura 331:41-46 (1998)). Integrin α4β7 itself acts as a homing receptor that mediates lymphocyte migration to the lymphoid tissue of the intestinal mucosa (Schwelghoffer, T., et al., J. Immunol. 151: 717-729(1993)). Antibodies against human α4β7 integrin, such as the marine moldoclonal antibody Act-1 (mAb Act-1), interfere with the binding of α4β7 integrin to the mucosal addressin cell adhesion molecule 1 (MAdCAM-1) present in upper endothelial venules in mucosal lymph nodes. Act-1 was originally isolated by Lazarovits, AL, et al., J. Immunol. 133:1857-1862 (1984), from mice immunized with human tetanus toxoid-specific T lymphocytes and was reported as an IgG1 / K antibody. Subsequent analysis of the antibody by Schweighoffer, T., et al., J. Immunol. / 5 / :717729 (1993) demonstrated that it can bind to a subset of human memory CD4+ T lymphocytes that selectively express the integrin α4β7. Entyvio™ vedolizumab, a monoclonal antibody 5 (mAb).Vedolizumab, an anti-α«β» integrin with structural features derived from Act-1, is indicated for the treatment of ulcerative colitis (UC) and Crohn's disease (CD). Studies indicating the activity of vedolizumab in treating these disorders (Feagen et al. NEJM 369:699-710 (2013) and Sandbom et al. NEJM 369:711-721 (2013)) showed varying levels of success depending on the disorder and the nature of prior therapies. Although growth dysfunction is a common sequela of ulcerative colitis and Crohn's disease in the pediatric population, pediatric patients appear to have twice the risk of growth dysfunction as patients with ulcerative colitis (Motil et al., Gastroenterology 105:681-691 (1993).). Nutritional therapy and resection have been observed to improve growth, but there remains a clear need for more effective and less morbid treatment options for the pediatric patient population. BRIEF DESCRIPTION OF THE INVENTION The invention relates to the treatment of pediatric patients suffering from inflammatory bowel disease (IBD), for example, Crohn's disease (CD) or ulcerative colitis (UC), and to the use of an αα4β7 integrin antagonist for the relief of IBD symptoms. In one aspect, the pediatric patient has moderate to severe UC or CD. In one aspect, the methods comprise administering an anti-integrin antibody, such as an αα4β7 integrin antibody, such as vedolizumab. In one respect, the pediatric patient who has inflammatory bowel disease has an inadequate response, loss of adequate response, or intolerance to at least one of the following: corticosteroids, immunomodulators, and / or tumor necrosis factor alpha (TNF-ct) antagonist therapy. In one aspect, the invention relates to a method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient with IBD of: a first 100 mg dose of an antibody having binding specificity for human integrin α4β7, a second 100 mg dose of the antibody two weeks after the first dose, and a third 100 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO: 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO: 2. The method may further comprise a fourth 100 mg dose at 14 weeks after the first dose.The method may further comprise a fifth and subsequent doses of 100 mg every eight weeks after the fourth dose. The method may further comprise a fifth and subsequent doses of 200 mg every eight weeks after the fourth dose. The antibody heavy chain may comprise amino acids 20 to 470 of SEQ ID NQ:1 and the antibody light chain may comprise amino acids 20 to 238 of SEQ ID NOS. Each dose may be administered intravenously as an infusion over approximately 120 minutes. The pediatric patient may weigh less than 30 kg. Inflammatory bowel disease may be moderate to severe Crohn's disease. Inflammatory bowel disease may be moderate to severe ulcerative colitis.The pediatric patient may have had an inadequate response, loss of response, or intolerance to a TNFα antagonist. The pediatric patient may have had an inadequate response or loss of response to a corticosteroid. The pediatric patient may have had an inadequate response or loss of response to an immunomodulator. Clinical response may be achieved by week 14. The pediatric patient may achieve remission of inflammatory bowel disease. In another aspect, the invention relates to a method for treating intestinal disease Inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient with IBD of: a first 200 mg dose of an antibody having binding specificity for human integrin α4β7, a second 200 mg dose of the antibody two weeks after the first dose, and a third 200 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO: 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO: 2. The method may further comprise a fourth 200 mg dose at 14 weeks after the first dose. The method may further comprise a fifth and subsequent 200 mg doses every eight weeks after the fourth dose.The antibody heavy chain may comprise amino acids 20 to 470 of SEQ ID NO:1, and the antibody light chain may comprise amino acids 20 to 238 of SEQ ID NO:2. Each dose may be administered intravenously as an infusion over approximately 120 minutes. The pediatric patient may weigh less than 30 kg. Inflammatory bowel disease may be moderate to severe Crohn's disease. Inflammatory bowel disease may be moderate to severe ulcerative colitis. The pediatric patient may have had an inadequate response, loss of response, or intolerance to a TNFα antagonist. The pediatric patient may have had an inadequate response or loss of response to a corticosteroid. The pediatric patient may have had an inadequate response or loss of response to an immunomodulator. Clinical response may be achieved by week 14.The pediatric patient can achieve a remission of 30: inflammatory bowel disease. In another aspect, the invention relates to a method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of a first 150 mg dose of an antibody having binding specificity for human integrin α4β7, a second 150 mg dose of the antibody two weeks after the first dose, and a third 150 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO: 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO: 2. The method may further comprise a fourth dose of 150 mg at 14 weeks after the first dose. The method may further comprise a fourth dose of 300 mg at 14 weeks after the first dose. The method may further comprise a fifth and subsequent doses of 150 mg every eight weeks after the fourth dose. The method may further comprise a fifth and subsequent doses of 300 mg every eight weeks after the fourth dose. The antibody heavy chain may comprise amino acids 20 to 470 of SEQ ID NO. 1 and the antibody light chain may comprise amino acids 20 to 238 of SEQ ID NO. 2. Each dose may be administered intravenously as an infusion over approximately 30 minutes. The pediatric patient may weigh 30 kg or more. Inflammatory bowel disease may be moderate to severe Crohn's disease.Inflammatory bowel disease (IBD) 10 may be moderate to severe ulcerative colitis. The pediatric patient may have had an inadequate response, loss of response, or intolerance to a TMF antagonist. The pediatric patient may have had an inadequate response or loss of response to a corticosteroid. The pediatric patient may have had an inadequate response or loss of response to an immunomodulator. Clinical response may be achieved by week 14. The pediatric patient 15 may achieve remission of IBD. In another aspect, the invention relates to a method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient with IBD of a first 300 mg dose of an antibody having binding specificity for human α4β7 integrin, a second 300 mg dose of the antibody two weeks after the first dose, and a third 300 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO: 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO: 2. The method may further comprise a fourth 300 mg dose at 14 weeks after the first dose. The method may further comprise a fifth and subsequent 300 mg doses every eight weeks after the fourth dose.The antibody heavy chain may comprise amino acids 20 to 470 of SEQ ID NG:1, and the antibody light chain may comprise amino acids 20 to 238 of SEQ ID NO:2. Each dose may be administered intravenously as an infusion over approximately 30 minutes. The pediatric patient may weigh 30 kg or more. Inflammatory bowel disease may be moderate to severe Crohn's disease. Inflammatory bowel disease may be moderate to severe ulcerative colitis. The pediatric patient may have had an inadequate response, loss of response, or intolerance to a TNFα antagonist. The pediatric patient may have had an inadequate response or loss of response to a corticosteroid. The pediatric patient may have had an inadequate response or loss of response to an immunomodulator. Clinical response may be achieved by week 14.The pediatric patient can achieve remission of inflammatory bowel disease. In another aspect, the invention relates to a method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of a first 100 mg dose of an antibody having binding specificity for human integrin α4β7, a second 100 mg dose of the antibody two weeks after the first dose, and a third 100 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of a human-derived antibody, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain CDR1 SEQ ID NO:7, CDR2 SEQ ID NO:8, and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NQ:4, CDR2 SEQ ID NO:5 and CDR3SEQ ID NO:6. In another aspect, the invention relates to a method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of: a first 200 mg dose of an antibody having binding specificity for human integrin α4β7, a second 200 mg dose of the antibody two weeks after the first dose, and a third 200 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO:7, CDR2 SEQ ID NO:8 and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NO:5 and CDR2 SEQ ID NO:5 and CDR3 SEQ ID NO:6. In another aspect, the invention relates to a method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of a first 150 mg dose of an antibody having binding specificity for human α4β7 integrin, a second 150 mg dose of the antibody two weeks after the first dose, and a third 150 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO. 7, CDR2 SEQ ID NO. 8, and CDR3 SEQ ID NO. 9; and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5 and CDR3 SEQ ID NO:6 In another aspect, the invention relates to a method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of a first dose of 380 mg of an antibody having binding specificity for human integrin α4β7, a second dose of 300 mg of the antibody two weeks after the first dose, and a third dose of 300 mg of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO:7, CDR2 SEQ ID NO:8 and CDR3 SEQ ID NO:8; and heavy chain; CDR1 SEQ ID NO:4, CDR2- SEQ ID NO:5 and CDR3 SEQ ID NO:6. Subsequent doses of the antibody can be administered subcutaneously.Each subcutaneous dose can be 108 mg of antibody. The subcutaneous dose can be administered every two or four weeks to a pediatric patient weighing 30 kg or more. The subcutaneous dose can be administered every three, four, five, six, seven, eight, nine, or ten weeks to a pediatric patient weighing between 10 kg and 30 kg. In another aspect, the invention relates to a method for treating inflammatory bowel disease (IBD) in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of: a first dose of 200 mg of an antibody having binding specificity for human integrin α4β7, a second dose of 200 mg of the antibody two weeks after the first dose, and subcutaneous administration of a third dose of 108 mg of the antibody six weeks after the first dose and subsequent doses of 108 mg of the antibody every two, three, or four weeks thereafter, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex.where the antigen-binding region comprises the following 15 CDRs: light chain: CDR SEQ ID NO:7, CDR2 SEQ ID NO:8 and CDR3 SEQ ID NO:9: and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5 and CDR3 SEQ ID NO:6. In another aspect, the invention relates to a method for treating a pediatric cancer patient undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT), comprising intravenously administering to a pediatric patient the day before the allo-HSCT a first dose of 200 mg of an antibody having binding specificity for human α4β7 integrin, a second dose of 200 mg of the antibody two weeks after the first dose, and subcutaneously administering a third dose of 108 mg of the antibody six weeks after the first dose and subsequent doses of 108 mg of the antibody every two, three, or four weeks thereafter, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin.where the antibody has a binding specificity for the complex where the antigen-binding region comprises the following CDRs: light chain: CDR SEQ ID NO:7, CDR2 SEQ ID NO:8 and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5 and CDR3 SEQ ID NO:6. In another aspect, the invention relates to a method for treating a pediatric patient with a monogenic defect with IBD-like pathology, comprising the intravenous administration to the pediatric patient of: a first dose of 200 mg of an antibody having binding specificity for human integrin α4β7, a second dose of 200 mg of the antibody two weeks after the first dose, and a third dose of 200 mg of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain: CDR SEQ ID NO:7, CDR2 SEQ ID NO:8, and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5 and CDR3 SEQ ID NO:6.The monogenic defect with IBD-like pathology may be glycogen storage disease type 1b, IL10 loss of function and mutations in IL10 or IL10 receptors, X-linked immunoproliferative syndrome 2, IPEX syndrome caused by mutations in the FOXP3 transcription factor, or chronic granulomatous disease. Method B may further comprise a subsequent dose of 200 mg every eight weeks thereafter. Method 5 may further comprise a subsequent dose of 200 mg until the pediatric patient weighs 30 kg or more. In another aspect, the invention relates to a vial manufactured to administer 200 mg of an anti-a4b7 antibody for the treatment of a pediatric patient. Any of the methods described herein comprising a dose of 100 mg, 200 mg or 150 mg may further comprise increasing the dose to 300 mg after pediatric patients weigh 30 kg or more. The antibody used in the methods described herein may be a humanized antibody. The humanized antibody may comprise a heavy chain variable region sequence of amino acids 20 to 140 from SEQ ID NO: 1 and a light chain variable region sequence of amino acids 20 to 131 from SEQ ID NO: 2. BRIEF DESCRIPTION OF THE FIGURES Figure 1 shows a schematic of a study design. The study includes a four-week assessment period and a 22-week double-blind treatment period (with the last dose at week 14 for all subjects). After the four-week assessment period, the 20 subjects weighing 30 kg or more receive a dose at weeks 0, 2, 6, and 14 of either 300 mg or 150 mg of vedoiizumab intravenously. Subjects weighing less than 30 kg receive a dose at weeks 0, 2, 6, and 14 of either 200 mg or 100 mg of vedoiizumab intravenously. A visit to administer a nanodose between days 16 and 42 may be scheduled for pharmacokinetic data collection. Subjects who consent to participate in the open-label extension (OLE) study may be eligible for OLE dosing after the procedures have been completed at week 22 (visit 9).Subjects who do not enter the OLE study or who withdraw before week 22 will also complete the final visit (week 22) and a final safety visit 18 weeks after their last dose of the study drug. Subjects who withdraw before week 22 will also participate in a 30-week long-term follow-up safety survey by telephone six months after their last dose of the study drug. Subjects will provide informed / pediatric consent for participation in the OLE study at week 14 of the study—or after completing it. Subjects who did not enter the OLE study will complete the final safety visit 18 weeks after their last dose of the study drug and participate in the long-term follow-up safety survey by telephone six months after their last dose of the study drug. Figure 2 is a schematic of a second study design. This study will begin after the week 22 visit for the study presented in Example 1 and Figure 1. Subjects receiving the low dose (150 mg for subjects 30 kg or more; 100 mg for subjects less than 30 kg) of IV vedoizumab may be switched to the higher dose (300 mg for subjects 30 kg or more; 200 mg for subjects less than 30 kg) at the investigator's discretion if the subject exhibits worsening disease as measured by PUCAI / PCDAI on two consecutive visits. Subjects who are dose-increased due to non-response should be given a dose based on their weight at the time of non-response in the study of Example 1, Figure 1. DETAILED DESCRIPTION The invention relates to methods for treating a pediatric patient with inflammatory bowel disease (IBD) with an α4β7 integrin antagonist, such as an α4β7 antibody, for example, vedoizumab, and methods for maintaining IBD remission in a pediatric patient. The invention further relates to methods for treating a pediatric patient with or at risk of graft-versus-host disease (GvHD), a pediatric patient with a monogenic defect with IBD-like pathology, a pediatric patient with glycogen storage disease type 1b, a pediatric patient with IL10-related loss-of-function colitis and mutations in IL10 or IL10 receptors, a pediatric patient with X-linked lymphoproliferative syndrome (XIAP gene defect),A pediatric patient with IPEX syndrome caused by mutations in the FOXP3 transcription factor, a pediatric patient with very early-onset inflammatory bowel disease (onset <6 years of age), a pediatric patient with indeterminate colitis (IBDU), and a pediatric patient with colitis associated with chronic granulomatous disease. The invention further relates to methods for treating a pediatric patient with a monogenic defect with IBD-like pathology with an α4β7 antagonist, such as an anti-α4β7 antibody, for example, vedoizumab. The monogenic defect may be a defect or a combination of epithelial response and epithelial barrier defects (for example, dystrophic epidermolysis bullosa, Kindier syndrome, X-linked immunodeficiency and ectodermal dysplasia, ADAM-17 deficiency, familial diarrhea); neutropenia and defects in bacterial destruction by phagocytes (for example, chronic granulomatous disease, glycogen storage disease type 1b, congenital neutropenia, leukocyte adhesion deficiency 1); hyper- and autoinflammatory disorders {e.g., mevanionate kinase deficiency, phospholipase Cy2 defects, familial Mediterranean fever, familial hematophagocytic lymphohistocytosis type 5, syndrome l.X-linked immunoproliferative disorder 2, X-linked immunoproliferative disorder 1, Hermansky-Pudlak syndrome); immune defects including T and B lymphocyte selection and activation defects, antibody and lymphocyte defects (e.g., Common Variable Immunodeficiency type 1, Common Variable Immunodeficiency type 8, agammaglobulinemia, hyper-IgM syndrome, Wiskott-Aidrich syndrome, Omenn syndrome, hyper-IgE syndrome, trichohepatoenteric syndrome; PTEN hamartoma tumor syndrome, Hoyera-Hreidarsson syndrome); T lymphocyte regulation and immunoregulation (X-linked immune dysregulation, polyendocrinopathy, enteropathy, IL10 signaling defects); and defects in intestinal innervation (e.g., disease of. Hirschspring). Vedolizumab, a humanized monoclonal antibody that specifically binds to αβζ integrin, is indicated for the treatment of patients with moderately to severely active ulcerative colitis (UC) and Crohn's disease (CD). Vedolizumab has a novel, gut-selective mechanism of action that differs from that of other currently marketed biologics for the treatment of inflammatory bowel disease (IBD), including natalizumab and tumor necrosis factor-α (TNF-α) antagonists. By binding to αβγ integrin expressed on the cell surface, vedolizumab blocks the interaction of a subset of intestinal memory T lymphocytes with mucosal addressin cell adhesion molecule 1 (MAdCAM-1) expressed on endothelial cells. Consequently, the migration of these cells to inflamed intestinal tissue is inhibited. The efficacy and safety of vedolizumab maintenance and induction therapy was demonstrated in adult patients with UC in the GEMINI 1 trial (ClinicalTrials.gov number NCT00783718) and in patients with CD in the GEMINI 2 (ClinicalTrials.gov number NCT00783692) and GEMINI 3 (ClinicalTrials.gov number NCT01224171) trials. More recently, several institutions around the world have completed studies using vedolizumab to treat pediatric patients. In one study, patients received vedolizumab intravenously at weeks 0, 2, and 6, and then approximately every eight weeks. The vedolizumab dose was fixed at 300 mg for 75% of the patients, but was dosed by weight for the remaining, smaller patients (Singó, et al., Inflammamm. Bowel Dis., 22(9):2121-2126, 2016). In another study, pediatric inflammatory bowel disease was treated in children aged 13 to 21 years. The adult dose of 300 mg was administered at weeks 0, 2, and 6, followed by a maintenance phase at 8-week intervals. Patients weighing less than 40 kg were excluded from the study. Contad, et al., Inflamm Bowel Dis., 22:2425-2431 (2016).Another study described administering the adult dose of 300 mg to 81% of the 25 children involved, while other children (weighing between 28.5 and 48 kg) received a reduced dose (3.6–10.3 mg / kg), Ledder et al., Journal of Crohn's and Colitis, 1230–1237 (2017). Therefore, there is clearly a desire to expand the use of vedolizumab for the treatment of pediatric patients. However, there is a need to develop a fixed dose that is suitable for smaller pediatric patients. Numerous adjustments for a smaller patient, especially a very young patient in a phase of life known for rapid growth, is an unnecessary burden and an opportunity for errors. A pediatric dosage for smaller patients is crucial to simplify the allocation of this patient population and avoid the potential for weight-based calculation errors. Definitions A “pediatric patient”, as used herein, refers to a human patient up to 18 years of age. As used herein, the “trough” level of serum concentration of an antibody refers to the concentration just before the next dose. “Clinical remission” or “remission”, as used herein with reference to subjects with ulcerative colitis, refers to a complete May score less than or equal to 2 points and no individual subscore greater than 1 point. “Clinical remission” of Crohn’s disease refers to a Crohn’s Disease Activity Index (CDAI) score of 150 or less, or an HBI score of 4 or less. The CDAI score weighs factors including the amount of loose or watery stools, the severity of abdominal pain, general well-being, extraintestinal manifestations of the disease such as arthritis, iritis, erythema, fistulas or abscesses, or fever, whether the patient is taking antidiarrheal medication, abdominal mass, hematocrit, and body weight. The Harvey-Bradshaw Index (HBI) is a simplified version of the CDAI for data collection purposes.It consists solely of clinical parameters, including general well-being, abdominal pain, amount of loose stool per day, abdominal mass, hematocrit, body weight, medications to control diarrhea, and the presence of complications, and requires only entries in a one-day diary. Magnetic resonance enterography (MRE) is being evaluated as a method to measure remission. “Endoscopic remission,” as used herein, refers to a condition with a low endoscopic score. An example of a method for assessing the endoscopic score in ulcerative colitis is flexible sigmoidoscopy. The endoscopic score in ulcerative colitis may include the Mayo subscore. An example of a method for assessing the endoscopic score in Crohn’s disease is ileocecal phenoscopy. The endoscopic score in Crohn’s disease may be the Simple Endoscopic Score for Crohn’s Disease (SES-CD). The SES-CD may include measurements such as ulcer size, the amount of ulcerated surface area, the amount of affected surface area, and whether and to what extent narrowing of the gastrointestinal tract occurred. A clinical response, as used herein with reference to subjects with ulcerative colitis, means a reduction in the full Mayo score of 3 points or more and 30% or more to 25 from the baseline value (or a partial Mayo score of 2 points or more and 25% or more from the baseline value, if the Mayo score was not performed at the visit) accompanied by a reduction in the rectal bleeding score of 1 point or more (>1) or an absolute rectal bleeding score less than or equal to 1 point (if).A “clinical response,” as used herein with reference to subjects with Crohn’s disease, refers to a decrease of 70 points or more in the CDAI score from the baseline value of 30 (week 0), a reduction of 50% or more in the SES-CD score from the baseline value, or is equal to an SES-CD score of 0 to 2 accompanied by a decrease in abdominal pain, or a decrease of 3 points or more from the baseline value of the HBI score. The terms “clinical response” and “response,” for example, alone or in combination with any adjective, are used interchangeably herein. “Endoscopic response,” as used herein, refers to a percentage decrease in an endoscopic score from a baseline value (e.g., during the evaluation or just before the initial dose). In Crohn’s disease, endoscopic response can be assessed using a simple endoscopic score for Crohn’s disease (SES-CD). “Reference value, as used herein, describes a parameter value that was measured before the initial dose of a treatment. It may refer to a measurement of a sample obtained on the same day, the day before, or during the week before the initial treatment; that is, in a period of time before the first dose when little change is expected until after the first dose, and measurement values ​​obtained after the first dose can be compared to this reference value to represent the change caused by the dose.” “Mucosal healing,” as used herein with reference to subjects with ulcerative colitis, refers to a Mayo endoscopic subscore less than or equal to 1. With reference to Crohn’s disease, mucosal healing refers to an improvement in the number or severity of mucosal lesions, e.g., in the digestive tract. For example, mucosal healing may refer to a decrease in the number, size, or severity of one or more ulcers in the digestive tract. In another example, mucosal healing refers to a decrease in one or more selected parameters from the group consisting of wall thickness, improvement of bowel wall contrast, mural edema, ulceration, and perienteric vascularity. Such mucosal healing may be expressed as an SES-CD score or a magnetic resonance activity index (MRA) score. Complete mucosal healing in Crohn’s disease includes the absence of ulceration. “PUCAl” or “Pediatric Ulcerative Colitis Activity Index,” as used herein, refers to the compilation of six clinical elements, including abdominal pain, rectal bleeding, consistency of most stools, number of stools per 24 hours, nocturnal stools (any episode that causes waking), and activity level. The PUCAl score ranges from 0 to 55; a score less than 10 indicates remission, 10 to 34 indicates mild disease, 35 to 64 indicates moderate disease, and 65 to 85 indicates severe disease. A clinically significant response is defined as a PUCAl change greater than or equal to 20. “PUCAl-based clinical response,” as used herein, refers to a decrease of 20 points or more from baseline in the Pediatric Ulcerative Colitis Activity Index (PUCAl) score. “PUCAl-based clinical remission,” as used herein, refers to a PUCAl score of less than 10. “Worsenration of disease,” as used herein, refers to a PUCAl increase greater than 20 points on two consecutive visits separated by at least seven days, or if the PUCAl is greater than 35 points on any scheduled or unscheduled visit (for subjects with ulcerative colitis): or a PCDAl increase greater than 15 points on two consecutive visits separated by at least seven days, or if the PCDAl is greater than 30 points on any scheduled or unscheduled visit. “PCDAI,” as used herein, refers to an assessment specifically designed for use with children. The PCDAI includes one child-specific component: height velocity, as well as three laboratory parameters: hematocrit (adjusted for age and sex), erythrocyte sedimentation rate (ESR), and albumin level. The PCDAI score ranges from 0 to 100, with higher scores indicating more active disease. A score below 10 is consistent with inactive disease. A score of 11 to 30 indicates mild disease, and a score above 30 indicates moderate to severe disease. A decrease of 12.5 points is considered evidence of improvement. Clinical remission based on the POCAS score is defined as a POCAS score of 10 or less. The “European 5-Dimensional Visual Analogue Scale (VAS) for Quality of Life (EQ-5.D),” as used herein, refers to a validated instrument (ahrq.gov / rice / eq5dproj.htm, “US. Valuation of the EuroQol EQ-5D™ Health States,” accessed August 8, 2012, Bastida et al. BMC Gastroenterology 10:26- (2010), Konig et al., European Journal of Gastroenterology & Hepatology 14:1205-1215 (2002)) used to measure health-related quality of life (HRQOL) in patients and includes five domains: mobility, self-care, usual activities, pain / discomfort, and Anxiety / Depression. Patients choose the level of health problems they currently have for each item as “none,” “moderate,” or “extreme”* and score themselves 1, 2, or 3, respectively. A composite EQ-5D score can be calculated from individual scores to assess overall HRQOL.The EQ-5D Visual Analog Scale (VAS) score is a self-assessed score of general health using a 20-cm vertical visual scale, with a score ranging from 0 (worst) to 100 (best) possible health. Many studies have shown that both the EQ-5D and VAS are valid and reliable instruments for measuring HRQOL in patients with glioblastoma. A decrease of >0.3 points in the EQ-5D score represents a clinically significant improvement in HRQOL for patients. An increase of 7 points or more in the VAS score also represents a clinically significant improvement in HRQOL for patients. The Inflammatory Bowel Disease Questionnaire (IBDQ) (Trvine Journal of Pediatric Gastroenterology & Nutrition 28:S23-27 (1999)) is used to assess quality of life in adult patients with inflammatory bowel disease, ulcerative colitis, or Crohn's disease, and includes 32 questions in four HRQOL areas: Intestinal Systems (10-25 questions), Emotional Functioning (12 questions), Social Functioning (5 questions), and Systemic Functioning (5 questions). Patients are asked to recall their symptoms and quality of life over the past 2 weeks and to rate each item on a 7-point Likert scale (higher scores indicate higher quality of life).A total IBDQ score is calculated by summing the scores for each domain; the total IBDQ score ranges from 32 to 224. A total IBDQ score greater than 170 is characteristic of a health-related quality of life (HRQoL) of patients in remission. As used herein, “induction therapy” is an initial stage of therapy where a patient is given a relatively intensive dosing regimen of a therapeutic agent. The therapeutic agent, for example, an antibody, is administered in a manner that rapidly provides an effective amount of the agent suitable for certain purposes, such as inducing immune tolerance to the agent or inducing a clinical response and improving the symptoms of the disease (see WO 2012 / 151.247 and WO 2012 / 151.248, which are incorporated herein by this reference). As used herein, a “maintenance therapy” occurs after induction therapy and is administered in a manner that continues the response achieved by the induction therapy with a stable level of therapeutic agent, e.g., antibody. A maintenance regimen may prevent the return of symptoms or recurrence of a disease, e.g., 1BD (see WO 2012 / 151247 and WO 2012 / 151248, which are incorporated herein by this reference). A maintenance regimen may provide convenience to the patient, e.g., it may be a simpler dosing regimen or require fewer visits for treatment. The cell surface molecule, “integrin ο4β7 or “α4β7, is a heterodimer of an accu chain (CD49D, ITGA4) and a β chain? (ITGB7). Each chain can form a heterodimer with an alternative integrin chain to form α^βι or οεβ?. The human genes cu and βγ (GenB'ank (National Center for Biotechnology Information, Bethesda, MD) (accession numbers RefSeq NM_000885 and NM_000889, respectively) are expressed by B and T lymphocytes, particularly CD4+ memory lymphocytes. As is typical for many integrins, α4β7 can exist in a resting or active state. Ligands for α4β7 include vascular cell adhesion molecule (VCAM), fibronectin, and mucosal addressin 1 (MAdCAM (e.g., MAdCAM-1)). The integrin α4β7 mediates lymphocyte trafficking to the GI mucosa and gut-associated lymphoid tissue (GALT) through adhesive interaction with mucosal addressin cell adhesion molecule 1 (MAdCAM-1), which is expressed on the endothelium of mesenteric lymph nodes and GI mucosa The term “antibody” is used herein in the broadest sense and specifically covers full-length monoclonal antibodies, immunoglobulins, polyclonal antibodies, multispecific antibodies (e.g., bispecific antibodies) formed from two full-length antibodies, e.g., each for a different antigen or epitope, and individual antigen-binding fragments, e.g., dAb, scFv, Fab, Ffab), Fab', including human, humanized, and non-human species antibodies, and recombinant antigen-binding forms of such monobodies and dibodies. As used herein, the term “monoclonal antibody” refers to an antibody obtained from a substantially homogeneous antibody population; that is, the individual antibodies comprising the population are identical and / or bind to the same epitope, except for possible variants that may arise during the production of the monoclonal antibody, which are generally present in minor quantities. Unlike polyclonal antibody preparations, which typically include different antibodies directed against different determinants (epitopes), each monoclonal antibody is directed against a single determinant on the antigen. The modifier “monoclonal” indicates the nature of the antibody obtained from a substantially homogeneous antibody population and should not be interpreted as requiring the production of the antibody by any particular method.For example, monoclonal antibodies for use according to the present invention can be prepared by the hybridization method, first described by Kohier et al., Nature, 256:495 (1975), or they can be prepared by recombinant DNA methods (see, for example, U.S. Patent No. 4,816,567). Monoclonal antibodies can also be isolated from phage antibody libraries by the techniques described in Claekson et al., Nature, 352:624-628 (1991); Marks et al., J. Mol. Biol., 222:581-597 (1991), for example. The antigen-binding fragments of an antibody comprise at least the variable regions of the heavy and / or light chains of an anti-C147 antibody. For example, the antigen-binding fragment of vedolzumab comprises amino acid residues 20-131 of the humanized light chain sequence SEQ ID NO:2. Examples of such antigen-binding fragments include Fab fragments, Fab' fragments, scFv fragments, and Ffbj fragments of a humanized antibody known in the art. The antigen-binding fragments of the humanized antibody of the invention can be produced by enzymatic cleavage or by recombinant techniques. For example, papain or pepsin cleavage can be used to generate Fab or Ffb'h fragments, respectively.Antibodies can also be produced in a variety of truncated forms by using antibody genes in which one or more stop codons have been introduced upstream of the natural termination site. For example, a recombinant construct encoding the heavy chain of an Ftabj fragment can be designed to include DNA sequences encoding the CH1 domain and the hinge region of the heavy chain. In one aspect, antigen-binding fragments inhibit the binding of α4β7 integrin to one or more of its antigens (e.g., mucosal addressin or MAdCAM (e.g., MAdCAM-1), fibronectin). The term “Fe receptor” or “FcR” is used to describe a receptor that binds to the Fe region of an antibody. In one respect, the FcR is a naturally occurring human FcR sequence. In another respect, the FcR binds to an IgG antibody (a gamma receptor) and includes receptors of the FcyRI, FcyRI1, and FcyRIIII subclasses, including allelic variants and alternative spliced ​​forms of these receptors. The FcyRI1 receptors include FcyRI1A (an “activating receptor”) and FcyRI1B (an “inhibitory receptor”), which have similar amino acid sequences that differ primarily in their cytoplasmic domains. The activating receptor FcyRI1A contains an activation motif based on the immunoreceptor tyrosine receptor (ITAM) in its cytoplasmic domain. The inhibitory receptor FcyRIIB contains an inhibitory motif based on the tyrosine immunoreceptor (ITIM) in its cytopiasmic domain. (See a review in M.Daeron, Annu. Rev. Immunol. 15:203-234 (1997)). The FcRs are reviewed in Ravetch and Kinet, Afína. R&v Immunol 9:457-92 (1991); Capel et al. , tmmunomethods 4:25-34 (1994); and de Haas et al., J. Lab. Clin. Med. 126:33-41 (1995). Other FcRs, including those that may be identified in the future, are encompassed by the term “FcR” at present. The term also includes the neonatal receptor, FcRn, which is responsible for the transfer of maternal IgG to the fetus (Guyer et al., J. Clin. Immunol. 117:587 (1976) and Kim et al., J. Immunol. 24:249 (1994)) and for the regulation of the persistence of immunoglobulin G (IgG) and albumin in serum (see a review in Rath et al., J. Clin. Immunol. 33Supp. 1:59-17 (2013)). The expression “hypervariable region” when used herein refers to amino acid residues of an antibody that are responsible for binding to the antigen and are found in the “variable domain” of each chain. The hypervariable region generally comprises amino acid residues from a complementarity-determining region or CDR (e.g., residues 24-34 (L1), 50-56 (L2) and 89-97 (L3) in the light chain variable domain and 31-35 (H1), 50-65 (H2) and 95-102 (H3) in the heavy chain variable domain; Kabat et al., Sequences of Proteins of Immunological Interest, 5th Ed. Public Health Service, National Institutes of Health, Bethesda, Md. (1991)) and / or residues from a “hypervariable loop” (e.g., residues 26-32 (L1), 50-52 (L2) and 91-96 (L3) in the light chain variable region and 26-32 (H1), 53-55 (H2) and 96-101 (H3) in the heavy chain variable domain). in the heavy chain variable region; Chothia and Lesk J Mol. Βίοι. f96:901-917 (1987))."Framework region" or "FR" residues are those variable domain residues other than hypervariable region residues as described herein. The hypervariable region or its CDRs can be transferred from one antibody chain to another or to another protein to confer binding specificity to the resulting antigen, antibody (compound), or binding protein. An “isolated” antibody is one that has been identified and separated and / or recovered from a component of its natural environment. In certain modalities, the antibody will be purified (1) to more than 95 wt% protein, as determined by the Lowry method and, alternatively, more than 99 wt%, (2) to a point sufficient to obtain at least 15 residues of the internal or N-terminal amino acid sequence, by using a rotating cup sequencer, or (3) to homogeneity by SDS-PAGE under reducing or non-reducing conditions, by using Coomassie blue or silver dye. The isolated antibody includes the antibody residing within recombinant cells since at least one component of the antibody's natural environment will not be present. Generally, however, the isolated antibody will be prepared by at least one purification step. “Treatment” refers to both therapeutic treatment and prophylactic or preventive measures. Those who need treatment include those who already have the disease, as well as those in whom the disease or its recurrence must be prevented. Therefore, the patient to be treated in this document may have been diagnosed as having the disease or may be predisposed to, or susceptible to, the disease. The terms “patient” and “subject” are used interchangeably herein. The expression “around” means that the value that follows it may be the midpoint of an interval, such as + / -5% of the value. If the value is a relative value given in percentages, the expression “around” indicates that the value that follows it may not be exact, but is the midpoint of an interval of + / -5% of the value, where the upper limit of the interval cannot exceed a value of 100%. Treatment of subjects with inflammatory bowel disease with anti-β4γ7 antibodies. In one aspect, the invention relates to methods for treating IBD (e.g., ulcerative colitis (UC), Crohn's disease (CD)) in a pediatric subject comprising administering to the pediatric subject an anti-β4γ7 antibody described herein in an amount effective to treat IBD, for example, in a child or adolescent. The pediatric patient or subject may be an adolescent or a child (e.g., from 2 to 17 years of age, inclusive). A pharmaceutical composition comprising an anti-β4γ7 antibody may be used as described herein to treat IBD in a pediatric patient suffering from it. The pediatric patient may have moderately to severely active UC or CD.For example, the pediatric patient may have a total Mayo score of 6 to 12 and a total Mayo subscore of stool frequency and rectal bleeding ≤4 and an endoscopic subscore ≥2, or have moderately to actively active CD defined as an Endoscopic Score for Crohn's Disease (SES-CD) ≥7, and the components of the Crohn's Disease Active Index (CDAI) of average daily abdominal pain score >1 for the preceding 7 days, and a total amount of loose / very soft stool >10 for the 7 days preceding the first dose of a treatment described herein. In some modalities, the CD suffered by the pediatric patient is close to the rectum, e.g., pancreatitis, not limited to proctitis. In some modalities, the CD suffered by the pediatric patient involves the ileum and / or the colon. In some forms, if the pediatric patient also suffers from structuring and penetration of the disease into the mucosa.The pediatric patient suffering from UC or CD may also have a growth deficiency. In some modalities, the pediatric patient suffering from CD has a mutation in the gene of the nucleotide-binding oligomerization domain-containing protein 2 (NOD2 / CARD15) (NCBI GenelD no. 64127, GenBank accession no. of the longer isotherm is ÑM_O22162 and of the shorter isotherm is NM_01293557). In some modalities, the pediatric patient suffering from CD has an antineutrophil cytoplasmic antibody or an anti-Saccharomyces cerevisiae antibody in circulation. In one aspect, the pediatric patient is 18 years of age or younger. In some modalities, the pediatric patient is between approximately 2 and approximately 17 years of age, between approximately 2 and approximately 14 years of age, between approximately 2 and approximately 10 years of age, between approximately 2 and approximately 8 years of age, between approximately 10 and approximately 18 years of age, between approximately 8 and approximately 14 years of age, between approximately 11 and approximately 15 years of age, or between approximately 13 and approximately 17 years of age. The anti-o4p7 antibody for use in the methods or uses provided herein can bind to an epitope on the α4 chain (e.g., humanized MAb 21.6 (Bendig et al., U.S. Patent No. 5,840,299)), on the 'o7 chain (e.g., FIB504 or a humanized derivative (e.g., Fong et al., U.S. Patent No. 7,528,236)), or to a combinatorial epitope formed by the association of the α4 chain with the 'o7 chain. In one respect, the antibody is specific for the o4p7 integrin complex, e.g., it binds to a combinatorial epitope on the α4β7 complex, but it does not bind to an epitope on the o4 chain or the 'o7 chain unless the chains are associated with each other. The association of integrin α4 with integrin δ7 can create a combinatorial epitope; for example, by bringing together residues present in both chains that together comprise the epitope, thus conformationally exposing on one chain, for example, the integrin δ4 chain or the integrin δ7 chain, an epitope binding site that is inaccessible to antibody binding in the absence of the appropriate integrin partner or in the absence of integrin activation. In another aspect, the antibody anti-α407 binds to both the integrin α4 chain and the integrin δ7 chain and is therefore specific for the integrin δ407 complex. Combinatorial epitope anti-α407 antibodies can bind to α407 but not to α401, and / or not to αεβ7, for example. -In another aspect, the anti-a407 antibody binds to the same or substantially the same epitope as the Act-1 antibody (Lazarovits, A. i. et al., J. Immunal,. 133(4): 1857-1862. (1984), SchWeíghoffér et al., J.Immunal, 151(2): 717-729, 1993; Bednarczyk et al. J. Biol. Chem., 269(11): 8348-8354, 1994). The marine hypridomide cell line ACT-1, which produces the mono-antibody Act-1 marine, was deposited in accordance with the provisions of the Budapest Treaty on August 22, 2001, on behalf of Millennium Pharmaceuticals, Inc., 40 Landsdowne Street, Cambridge, Mass. 02139, USA, in the American Type Culture Collection, 10801 University Boulevard, Manassas, Va. 20110-2209, USA, with accession number PTA-3663. In another respect, the anti-o4P7 antibody is a human antibody or α4β7 binding protein that uses the CDRs provided in US patent application publication no. 2010 / 0254975. In one aspect, the anti-q4P7 antibody inhibits the binding of α4β7 to one or more of its ligands (e.g., mucosal addressin, e.g., MAdCAM-1, fibrillonectin, and / or vascular addressin (VCAM)). Primate MAdCAM is described in PCT publication WO 96 / 24673, the Indications of which are incorporated herein in full by reference. In another aspect, the anti-α4β7 antibody inhibits the binding of α4β7 to MAdCAM (e.g., MAdCAM-1) and / or fibrillonectin without inhibiting VCAM binding. In another aspect, the anti-integrin antibody, e.g., anti-α4β7, which has binding specificity, e.g., comprising the complementarity-determining regions of the mouse Act-1 antibody.For example, a humanized anti-o487 antibody comprises a heavy chain containing the three heavy chain complementarity-determining regions (CDRs, CDR1, SEQ ID NO:4, CDR2, SEQ ID NO:5, and CDR3, SEQ ID NO:6) of the mouse Act-1 antibody and the appropriate human heavy chain framework regions; and also comprises a light chain containing the three light chain CDRs (CDR1, SEQ ID NO:7, CDR2, SEQ ID NO:8, and CDR3, SEQ ID NO:9) of the mouse Act-1 antibody and appropriate human light chain framework regions. In some embodiments, the anti-o4p7 antibody is an isotype of IgG1. In other embodiments, the 3πΐί-α4β7 antibody is an isotype of IgG2, IgG3, or IgG4. In one respect, the anti-d4p7 antibodies used in treatments are humanized versions of the mouse Act-1 antibody. Appropriate methods for preparing humanized antibodies are known in the art. Generally, the humanized anti-d4p7 antibody will contain a heavy chain containing the three heavy-chain complementarity-determining regions (CDRs, CDR1, SEQ ID NO:4; CDR2, SEQ ID NO:5; and CDR3, SEQ ID NO:6) of the mouse Act-1 antibody and the appropriate human heavy-chain framework regions; and it will also contain a light chain containing the three light-chain CDRs (CDR1, SEQ ID NO:7; CDR2, SEQ ID NO:8; and CDR3, SEQ ID NO:9) of the mouse Act-1 antibody and appropriate human light-chain framework regions. The humanized Act-1 antibody may contain any appropriate human framework regions, including consensus framework regions, with or without amino acid substitutions.For example, one or more of the framework amino acids can be replaced with another amino acid, such as the amino acid at the corresponding position in the mouse Act-1 antibody. The human constant region, or part of it if present, can be derived from the κ or λ light chains and / or the heavy chains of human antibodies (e.g., y1, y2, y3, y4), μ, α (e.g., a1, a2), δ, or even allelic variants. A particular constant region (e.g., lgG1) variant, or parts thereof, can be selected to construct the voting function. For example, a mufed constant region (variant) can be incorporated into a fusion protein to minimize binding to Fe receptors and / or the ability to fix complement (see, for example, Winter et al., GB 2,209,757 B; Morrison et al., WO 89 / 07142; Morgan et al., WO 94 / 29351, 22 Dec. 5, 1994). Humanized versions of the Act-1 antibody are described in PCT publications no. WO98 / 06248 and WO07 / 61679, the content of which is incorporated in its entirety herein by means of this reference. In one aspect, the anti-~o407 antibody is vedolizumab. Vedolizumab (also called MLN0002, ENTYVIO™, or KYNTELES™) is a humanized immunoglobulin (Ig) G1 mAb directed against α4β7 integrin on human lymphocytes. Vedolizumab binds to α4β7 integrin, antagonizes its adherence to MAdCAM-1, and thus impedes the migration of intestinal homing leukocytes to the GI mucosa. Vedolizumab is an integrin receptor antagonist indicated for adult patients with moderately to severely active ulcerative colitis (UC) or dengue fever (CD) who have had an inadequate response, loss of response, or intolerance to an immunomodulator or tumor necrosis factor (TNF) blocker, or who have had an inadequate response, intolerance, or dependence on corticosteroids.For ulcerative colitis (UC), vedolizumab is used to induce and maintain a clinical response, induce and maintain clinical remission, improve the endoscopic appearance of the mucosa, and / or achieve corticosteroid-free remission. For dengue hemorrhagic fever (DC), vedolizumab is used to achieve a clinical response, achieve clinical remission, and / or achieve corticosteroid-free remission. In some modalities, corticosteroid-free remission is achieved through a tapering regimen during continuous vedolizumab treatment. In another aspect, humanized anti-O4p7 antibodies for use in treatment comprise a heavy chain variable region comprising amino acids 20-140 of SEQ ID NO:1, and a light chain variable region comprising amino acids 20-131 of SEQ ID NO:2 or amino acids 21-132 of SEQ ID NO:3. If desired, one or more suitable human constant regions may be present. For example, the humanized anti-O4p7 antibody may comprise a heavy chain comprising amino acids 20-470 of SEQ ID NO:1 and a light chain comprising amino acids 21-239 of SEQ ID NO:3. In another example, the humanized anti-O407 antibody may comprise a heavy chain comprising amino acids 20 to 470 of SEQ ID NO:1 and a light chain comprising amino acids 20 to 238 of SEQ ID NO:2. The humanized light chain of vedolizumab (e.g., Chemical Abstract Service (CAS, (American Chemical Society) registration no. 943609-66-3), with two mouse residues replaced by human residues, is more human than the light chain of LDP-02, another humanized anti-o4p7 antibody. In addition, LDP-02 has a somewhat hydrophobic, flexible alanine 114 and a hydrophilic site (Aspartate 115) that is replaced in vedolizumab with the slightly hydrophilic hydroxyl-containing threonine 114 and the potentially inward-facing valine 115 residue. Additional substitutions to the anti-o467 antibody sequence may be, for example, mutations in the light and heavy chain frame regions, such as an isoleucine to valine mutation at residue 2 of SEQ 10 NO: 10; a methionine to valine mutation at residue 4 of SEQ l'D NO: 10; an alanine to glycine mutation at residue 24 of SEQ ID NO: 11;.an arginine-to-lysine mutation at residue 38 of SEQ ID NO:11; an alanine-to-arginine mutation at residue 40 of SEQ ID NO:11; a methionine-to-iscleucine mutation at residue 48 of SEQ ID NO:11; an iscleucine-to-leucine mutation at residue 69 of SEQ ID NO:11; an arginine-to-valine mutation at residue 71 of SEQ ID NO:11; a threonine-to-iscleucine mutation at residue 73 of SEQ ID NO:11; or any combination thereof; and the replacement of the heavy chain CDRs with the CDRs (CDR1, SEQ ID NO:4, CDR2, SEQ ID NO:5 and CDR3, SEQ ID NO:6) of the mouse Aet-1 antibody; and the replacement of the light chain CDRs with the light chain CDRs (CDR1, SEO ID NO:7, CDR2, SEQ ID NO:8 and CDR3, SEQ ID NO:9) of the mouse Act-1 antibody. In one aspect, the humanized antba437 antibody for use in the treatment of a pediatric human patient is included in a stable formulation comprising a mixture of a non-reducing sugar, an anti-o4p7 antibody, and at least one free amino acid (i.e., not bound to a protein), and the molar ratio of the reducing sugar to the anti-a487 antibody (mol / mol) is greater than 650:1. The formulation may be a liquid formulation or a dry formulation (e.g., lyophilized). The formulation may also contain a buffering agent. In some embodiments, the non-reducing sugar is mannitol, sorbitol, sucrose, trehose, or a combination thereof. In some formulations, the free amino acid is histidine, arginine, arginine, glycine, glutamic acid, or any combination thereof. The formulation may comprise between approximately 50 mM and approximately 175 mM of free amino acid. The ratio of free amino acid to antibody molar ratio may be at least 250:1, from 200:1 to 500:1, or from 250:1 to 400:1. The formulation may also contain a surfactant. The surfactant may be polysorbate 20, polysorbate 80, a poloxamer, or a combination thereof. The surfactant may have a concentration of between approximately 0.2 mg / ml and 2.5 mg / ml, between approximately 0.4 mg / ml and 0.5 mg / ml, between approximately 0.5 mg / ml and 0.8 mg / ml, or between approximately 1.8 mg / ml and 2.2 mg / ml. In some embodiments, the surfactant concentration is approximately 0.6 mg / ml. In some embodiments, the surfactant concentration is approximately 0.75 mg / ml. In some embodiments, the surfactant concentration is approximately 2.0 mg / ml. In some aspects, the formulation may minimize the immunogenicity of the anti-α4β7 antibody. The formulation, for example, in the dry state, can be stable for at least three months at 40°C and 75% relative humidity (RH). In the dry state, the lyophilized formulation has between approximately 0.5% and 10% moisture, between approximately 0.8% and 7.5%, between approximately 1% and 5%, <5%, <4%, 3%, or <2.5% moisture, for example, as determined by Karl Fischer titration. Upon reconstitution, for example, after storage at 25°C, 30°C, or 2–8°C, a stable lyophilized formulation comprises approximately 0–10% of aggregated anti-α4p7 antibody (e.g., dimers, trimers, or multimeric forms of the antibody and / or antibody degradation products, as measured by size exclusion chromatography). In some forms, the stored reconstituted lyophited formulation of the anti-o4p7 antibody comprises between approximately 0% and 5.0%, 0% and 2%, <2%, or <0.5% of aggregates. In another aspect, the formulation is lyophilized and comprises at least approximately 5% to 10% w / w of anti-α4β7 antibody before lyophilization. The formulation may contain at least approximately 6% w / w of anti-α4β7 antibody before lyophilization. The formulation can be reconstituted from a lyophilized formulation (e.g., reconstituted to comprise a stable liquid formulation). The dry formulation of an βηίί-α4β7 antibody comprises between approximately 25% and 35% w / w and between approximately 29% and approximately 32% w / w of anti-α4β7 antibody. The dry formulation of a 3πίί~α4β7 antibody may further comprise from about 30% to 65% w / w, from about 40% to 60%, from about 45% to 55%, or 50% to 52% w / w of anti-α4β7 reducing sugar, such as sucrose or trehalose.The dry formulation of an anti-u4,87 antibody may further comprise from about 5% to 20% w / w or from about 10% to about 15% w / w of an amino acid salt, such as arginine hydrochloride. The dry formulation may further comprise from about 1% to 10% w / w, from about 2% to 7% w / w, or from about 4% to 6% w / w of buffer, for example, histidine. In some embodiments, the dry formulation comprises from about 30% to 31% w / w of 3Pα4β7 antibody, for example, vedolizumab, from about 50% to 52% w / w of sucrose, and from about 12% to 14% w / w of arginine hydrochloride. The above dry formulations may further comprise between approximately 0.25% and 0.4% w / w, or between approximately 0.9% and 1.2% w / w of polysorbate 80. In another aspect, the invention relates to the treatment of a pediatric patient with a stable formulation comprising a mixture of a non-reducing sugar, an anti-a4p7 antibody and at least one free amino acid, and the molar ratio between the non-reducing sugar and the anti-a4p7 antibody (mohmol) is greater than 650:1 and the ratio between free amino acid and anti-a4p7 antibody (mokmol) is greater than 250:1. In another aspect, the invention relates to the treatment of a pediatric patient with a stable formulation comprising a mixture of a non-reducing sugar, an anti-α4β7 antibody and at least one free amino acid, and the molar ratio between the non-reducing sugar and the anti-α4β7 antibody (mokmoi) is greater than 650:1 and the ratio between free amino acid and anti-α4β7 antibody (moi:mol) is greater than 250:1. In another aspect, the invention relates to the treatment of a pediatric patient with a stable liquid formulation, for example, before cryophilization or after reconstitution with a solvent, comprising an aqueous solvent with a non-reducing sugar, an anti-δ4P7 antibody, and at least one free amino acid, wherein the molar ratio between the non-reducing sugar and the anti-δ4P7 antibody (mol:mol) is greater than 650:1. In a further aspect, the invention relates to a liquid formulation comprising at least about 40 mg / ml and about 80 mg / ml of anti-δ4P7 antibody, at least about 50-175 mM of one or more amino acids, and at least 6% and at least 11% (w / v) of sugar. The liquid formulation may also contain a buffering agent. A buffering agent may be histidine, succinate, phosphate, glycine, or citrate. In some forms, the liquid formulation also includes a metallic complainant.In some embodiments, the liquid formulation also includes an antioxidant, such as citrate. In some embodiments, the citrate concentration is between approximately 5 mM and 40 mM, between approximately 7.5 mM and 10 mM, or between approximately 20 and 30 mM. In some embodiments, the citrate concentration is approximately 25 mM. In some embodiments, the citrate concentration is approximately 9.4 mM. In another aspect, the invention relates to the treatment of a pediatric patient with a liquid formulation comprising at least approximately 60 mg / ml of 3ηϋ-α4β7 antibody, at least approximately 10% (w / v) of non-reducing sugar, and at least approximately 125 mM of one or more free amino acids. In some embodiments, the liquid formulation is approximately 60 mg / ml of anti-ct4p7 antibody. In another aspect, the invention relates to the treatment of a pediatric patient with a liquid formulation comprising at least about 60 mg / ml of anti-α4p7 antibody, at least about 10% (w / v) of non-reducing sugar, and at least about 175 mM of one or more free amino acids. In another additional aspect, the invention also relates to the treatment of a pediatric patient with a dry formulation, for example, lyophilized, comprising a mixture of a non-reducing sugar, an anti-a4p7 antibody, histidine, arginine and polysorbate 80, and the molar ratio between the non-reducing sugar and the anti-a4p7 antibody (mol:mol) is greater than 650:1. In another aspect, the invention relates to the treatment of a pediatric patient with a lyophilized formulation comprising a mixture of a non-reducing sugar, an anti-α4β7 antibody, histidine, arginine, and propyl sorbate 80. In this aspect, the molar ratio between the non-reducing sugar and the anti-α4β7 antibody (mol:mol) is greater than 650:1. Furthermore, the ratio between arginine and the anti-α4β7 antibody (mol:mol) in the formulation is greater than 250:1, and the molar ratio between histidine and arginine and the antibody (mol:mol) is from approximately 200:1 to approximately 500:1. In another aspect, the invention relates to the treatment of a pediatric patient with a stable liquid pharmaceutical formulation comprising a mixture of an anti-α4β7 antibody, citrate, histidine, arginine, and polysorbate 80. The formulation may be contained in a receptacle, such as a vial, cartridge, syringe, or autoinjector. In some embodiments, the liquid formulation comprises at least approximately 120 mg / ml of anti-α4β7 antibody, at least approximately 140 mg / ml of anti-α4β7 antibody, between 140 mg / ml and 250 mg / ml of anti-α4β7 antibody, between 140 mg / ml and 175 mg / ml of anti-α4β7 antibody, or between 150 mg / ml and 170 mg / ml of anti-α4β7 antibody. In other embodiments, the liquid formulation contains approximately 160 mg / ml of anti-α4β7 antibody. In one aspect, the humanized anti-a4p7 antibody for use in the treatment of pediatric patient 35 is lyophilized and stored as a single dose in a container, for example, a vial. The container, for example, a vial, is stored refrigerated, for example, at around 2-8°C or at room temperature, for example, between around 25°C and around 30°C, until administered to a subject in need. A container might be, for example, a 10 or 50 ec container (for example, for a dose of 60 mg / ml). The container, for example, a vial, may contain between approximately 90 and 115 mg, between approximately 95 and 105 mg, at least approximately 100 mg, between approximately 135 and 160 mg, between approximately 145 and 155 mg, at least approximately 150 mg, between approximately 180 and 220 mg, between approximately 190 and 210 mg, between approximately 195 and 205 mg.between at least around 200 mg, between around 280 mg and 320 mg, between around 290 mg and 310 mg, at least around 300 mg, between around 380 and 420 mg, between around 390 and 410 mg, or less around 400 mg, between around 580 and 620 mg, between around 590 and 610 mg, or less around 600 mg of anti-a437 antibody. In one aspect, the package contains about 200 mg of anti-α4β7 antibody. The vial may contain enough anti-α4β7 antibody, for example, vedolizumab, to allow the administration—for example, that it is manufactured to administer—about 100 mg, about 150 mg, about 200 mg, about 300 mg, about 400 mg, or about 600 mg of anti-α4β7 antibody. For example, the vial may contain about 15%, about 12%, about 10%, or about 8% more anti-α4β7 antibody than the dose amount. In another aspect, the anti-a437 antibody, for example, vedolizumab, for use in the treatment of a pediatric patient, is in a stable liquid pharmaceutical composition stored in a container, for example, a vial, syringe, or cartridge, at approximately 2–8°C until administered to the patient. The syringe or cartridge may be a container of 1 mL or 2 mL (for example, for a dose of 160 mg / mL) or larger than 2 mL, for example, for a higher dose (at least 320 mg or 400 mg or higher). The syringe or cartridge may contain at least approximately 20 mg, at least approximately 50 mg, at least approximately 70 mg, at least approximately 80 mg, at least approximately 100 mg, at least approximately 108 mg, at least approximately 12 mg.0 mg, at least around 155 mg, at least around 180 mg, at least around 200 mg, at least around 240 mg, at least around 300 mg, at least around 360 mg, at least around 400 mg, or at least around 500 mg of anti-a4p7 antibody. In some modalities, the container, e.g., syringe or can, may be manufactured to deliver between around 20 and 120 mg, between around 40 mg and 70 mg, between around 45 and 65 mg, between around 50 and 57 mg, or around 54 mg of anti-ci4>37 antibody, e.g., vedolizumab. In other modalities, the syringe or can can be manufactured to deliver between approximately 90 and 120 mg, between approximately 95 and 115 mg, between approximately 100 and 112 mg, or around 108 mg of anti-o4p7 antibody, for example, vedolizumab.In other modalities, the syringe or can can be manufactured to administer between approximately 149 and 250 mg, between approximately 150 and 200 mg, between approximately 160 and 170 mg, between approximately 160 and 250 mg, between approximately 175 mg and 210 mg, or around 160 mg, around 165 mg, around 180 mg, or around 200 mg of anti-a4P7 antibody, for example, vedolizumab. The present invention provides, in a first aspect, a method for treating a pediatric patient with inflammatory bowel disease (IBD) with an anti-q4p7 antibody, for example, vedolizumab. In this aspect, the method comprises administering an intravenous dose of vedolizumab. The dose may be 100 mg, 150 mg, 200 mg, or 300 mg of the anti-q4p7 antibody. In some embodiments, the dose may be selected based on the patient's weight. In one aspect, the pediatric patient weighs 30 kg or more. In another aspect, the pediatric patient weighs less than 30 kg. In some modalities, the pediatric patient who weighs 30 kg or more weighs between around 30 and 35 kg, between around 30 and 40 kg, between around 36 and 45 kg, between around 40 and 45 kg, between around 30 and 50 kg, or between around 40 and 50 kg.In other modalities, the pediatric patient who weighs less than 30 kg weighs between approximately 5 kg and 30 kg, between approximately 10 kg and 15 kg, between approximately 15 kg and 20 kg, between approximately 10 kg and 20 kg, between approximately 12 kg and 22 kg, between approximately 10 kg and 25 kg, between approximately 15 kg and 30 kg, or between approximately 10 kg and 30 kg. In some regimens, pediatric patients weighing less than 30 kg may be administered a dose of 100 mg to 200 mg of anti-α4p7 antibody. In some regimens, pediatric patients weighing 30 kg or more may be administered a dose of 150 mg to 300 mg of anti-α4p7 antibody. An anti-o4pβ antibody is administered in an effective amount to inhibit the binding of α4β7 integrin to its ligand. For therapeutic purposes, an effective amount will be sufficient to achieve the desired effect of response or remission (e.g., as defined herein). An α4β7 antagonist, such as an anti-o437 antibody, may be administered as a single dose or in multiple doses. Examples of routes of administration include topical routes, such as nasal, inhalation, or transdermal administration; enteral routes, such as via a feeding tube or suppository; and parenteral routes, such as intravenous, intramuscular, subcutaneous, intra-arterial, intraperitoneal, or intravitreal administration. Suitable doses may range from approximately 0.1 to 20 mg / kg of body weight to approximately 10.0 mg / kg of body weight, from approximately 1 mg / kg to approximately 60 mg / kg of body weight, from approximately 5 mg / kg to approximately 30 mg / kg of body weight, from approximately 6.5 mg / kg to approximately 20 mg / kg of body weight, or at least 15 mg / kg or at least 20 mg / kg of body weight per treatment. It is surprising that administering a fixed dose of 100 mg, 150 mg, or 200 mg, for example, from a dosage form, for example, a vial, manufactured to deliver between 95 and 110 mg, 100 mg, 108 mg, between 145 mg and 155 mg, 150 mg, between 155 mg and 170 mg, between 190 and 210 mg, or 200 mg of an anti-a407 antibody, for example, vedolizumab, to a smaller pediatric patient, for example, between 5 kg and 35 kg, between 10 kg and 30 kg, or less than 30 kg, is safe. In these modalities, smaller patients can be administered at least 20 mg / kg of an anti-α4p7 antibody, an unprecedented dose level in the therapeutic use of an anti-α4p7 antibody, for example, vedolizumab, where smaller adults are administered between around 5 and 7 mg / kg of anti-α4p7 antibody starting from a dose of 300 mg. However, the study in young monkeys showed the safety of the anti-α4p7 antibody, for example, vedolizumab, at doses up to 100 mg / kg. In some formulations, the 3ηδ-α4β7 antibody, such as vedolizumab, is provided as a dry lyophilized formulation that can be reconstituted with a liquid, such as sterile water, for administration. Administration of a reconstituted formulation can be by parenteral injection via one of the routes described above. An intravenous injection can be by infusion, or by additional dilution with isotonic saline, buffer, for example, phosphate-buffered saline, or Ringer's solution (lactic or dextrose). In some formulations, the anti-α4β7 antibody is administered by subcutaneous injection, for example, at a dose of approximately 54 mg, 108 mg, 165 mg, or 216 mg, every two, three, or four weeks after the start of therapy or after the third consecutive dose. In some modalities, vedolizumab is administered by intravenous injection, subcutaneous injection and / or infusion. In some formulations, vedolizumab is administered at a dose of 40 mg, 50 mg, 60 mg, 70 mg, 75 mg, 80 mg, 90 mg, 100 mg, 120 mg, 125 mg, 150 mg, 200 mg, 300 mg, 450 mg, 600 mg, 45-125 mg, 80-120 mg, 125-250 mg, or 90-210 mg. In some formulations, vedolizumab is administered, for example, subcutaneously, at a dose of 0.5 mg / kg, 1.0 mg / kg, 1.5 mg / kg, 2.0 mg / kg, 2.5 mg / kg, 3.0 mg / kg, 4.0 mg / kg, or 5.0 mg / kg, with a dose of 54 mg, 108 mg, 216 mg, 160 mg, 165 mg, 320 mg, or 480 mg. Vedolizumab can be administered once daily, weekly, monthly, or annually. A vedolizumab dosing regimen may have an initial or induction phase and a maintenance phase.An induction phase can consist of one or more doses, for example, two, three, or four doses of high amounts or without prolonged intervals, such as one, two, three, or four weeks between doses. For example, an induction regimen might have two doses, one on day (week) zero and one on week 2 (day 14). A maintenance phase, for example, to maintain IBD remission, might have lower doses or doses spaced further apart than in the induction phase. In some modalities, maintenance dosing is every four weeks. Every 6 weeks, every 8 weeks, every 10 weeks, or every 12 weeks. In some regimens, vedolizumab is administered at zero, two, and six weeks (induction), and then every four or eight weeks thereafter (maintenance). Pediatric patients with IBD refractory to other therapies may require longer induction periods, for example, 8, 10, 12, or 14 weeks before starting maintenance therapy. In one modality, vedolizumab is administered intravenously at weeks 0, 2, and 6, and then subjects who do not achieve a clinical response (based on PUCAI / PCDAI) at week 14 will receive a double dose at week 14 (e.g., a patient who receives a 100 mg dose at weeks 0, 2, and 6, who does not achieve a clinical response at week 14, will be given a 200 mg dose at week 14; a patient who receives a 150 mg dose at weeks 0, 2, and 6, who does not achieve a clinical response at week 14, will be given a 300 mg dose at week 14). In one modality, vedolizumab is administered intravenously at weeks 0, 2, 6, and 14. In some modalities, vedolizumab is administered intravenously at weeks 0, 2, 6, and 14, then every four or eight weeks thereafter. In some modalities, vedolizumab is administered intravenously at weeks 0, 2, 6, 10, and 14, then every four or eight weeks thereafter. In some modalities, vedolizumab is administered once or more, and then at least one month, at least six months, or at least one year later, vedolizumab is administered again one or more times. In some regimens, 100 or 150 mg of vedolizumab may be administered by intravenous infusion at weeks zero, two, six, and fourteen, and then, at eight-week intervals thereafter, 260 or 300 mg, respectively (i.e., twice the previous dose), of vedolizumab may be administered intravenously. In some regimens, 180 or 150 mg of vedolizumab may be administered by intravenous infusion at weeks zero, two, and six, and then, at four or eight-week intervals thereafter, 200 or 300 mg, respectively (i.e., twice the previous dose), of vedolizumab may be administered intravenously. In some regimens, 100 or 150 mg may be administered.Vedolizumab may be administered by intravenous infusion at week zero and two, and then at week six, 200 or 300 mg, respectively (i.e., twice the previous dose) of vedolizumab may be administered by intravenous infusion, and then at four-week or 10-week intervals. Eight weeks after this, 200 or 300 mg of vedolizumab may be administered intravenously. In some modalities, if the pediatric patient is treated with vedolizumab at week zero, 2, 6, and 14 at a dose based on a weight less than 30 kg and during treatment grows to 30 kg or more, then the pediatric patient may be treated with a dose based on the higher weight. In some modalities, a pediatric patient treated with the low size-relative dose (150 mg for subjects 30 kg or more, 100 mg for subjects less than 30 kg) of the anti-a437 antibody may have their dose increased to receive a higher size-relative dose (300 mg for subjects 30 kg or more; 200 mg for subjects less than 30 kg) if the patient experiences a worsening of the disease. In some regimens, 200 or 300 mg of vedolizumab may be administered by intravenous infusion at week zero and two, 200 or 300 mg of vedolizumab may be administered by intravenous infusion at week six, and then at intervals of two, three, or four weeks. After this, vedolizumab may be administered subcutaneously, for example, at a dose of 54, 108, 165, or 216 mg. In some regimens, 100 or 150 mg of vedolizumab may be administered by intravenous infusion at week zero and two, 200 or 300 mg of vedolizumab may be administered by intravenous infusion at week six and 14, and then at intervals of two. Three or four weeks after this, vedolizumab can be administered subcutaneously, for example, with a dose of 54, 108, 165, or 216 mg.In some modalities, 100 or 150 mg of vedolizumab can be administered by intravenous infusion in week zero and two, 200 or 300 mg of vedolizumab can be administered by intravenous infusion in week six, and then, at intervals of two, three, or four weeks thereafter, vedolizumab can be administered subcutaneously, for example, with a dose of 54, 108, 165, or 216 mg. In some regimens, 100 or 200 mg of vedolizumab can be administered by intravenous infusion to a patient weighing less than 30 kg or 10 kg less than 30 kg at weeks zero and two. 100 or 200 mg of vedolizumab can then be administered by intravenous infusion at weeks six and 35. Following this, at intervals of one, two, three, four, five, six, seven, eight, nine, or ten weeks, vedolizumab can be administered subcutaneously, for example, at a dose of 54, 108, 165, or 216 mg. In some regimens, the subcutaneous dose is 54 mg. In other regimens, the subcutaneous dose is 108 mg. In some regimens, 100 or 200 mg of vedolizumab can be administered by intravenous infusion to a patient weighing less than 30 kg or less than 30 kg at week zero and two. Then, 54, 108, 165, or 216 mg of vedolizumab can be administered subcutaneously at week six, and then, at intervals of one, two, three, four, five, six, seven, eight, nine, or ten weeks thereafter, vedolizumab can be administered subcutaneously, for example, at a dose of 54, 108, 165, or 216 mg. In some regimens, the subcutaneous dose is 54 mg. In other regimens, the subcutaneous dose is 108 mg. In some modalities, 300 mg of vedolizumab can be administered by intravenous infusion to a pediatric patient weighing 30 kg or more at week zero, two, and six, and then, at intervals of one, two, three, or four weeks thereafter, vedolizumab can be administered subcutaneously, for example, with a dose of 108 mg or 216 mg. In some modalities, 300 mg of vedolizumab can be administered by intravenous infusion to a pediatric patient weighing 30 kg or more at week zero, two, and then week six, and then, at intervals of one, two, three, or four weeks thereafter, vedolizumab can be administered subcutaneously, for example, with a dose of 108 mg or 216 mg. The interval between subcutaneous doses may be shorter for larger pediatric patients, e.g., those weighing 30 kg or more, so that they receive a subcutaneous dose at intervals of 1 to 6 weeks, and longer for smaller pediatric patients, e.g., those weighing less than 30 kg, or 10 kg less than 30 kg, so that they receive a subcutaneous dose at intervals of 3 to 20 weeks. In some modalities, the treatment method, dose, or dosing regimen reduces the likelihood of a patient developing a HAHA response to the anti-α4β7 antibody. The development of HAHA, as measured, for example, by antibodies reacting to the anti-α4β7 antibody, can increase the clearance of the anti-α4β7 antibody, for example, reduce the concentration of the anti-α4β7 antibody in the serum, for example, reduce the amount of anti-α4β7 antibodies bound to the α4β7 integrin, which would make the treatment less effective. In some modalities, to prevent the development of HAHA, the patient may be treated with an induction regimen followed by a maintenance regimen. In some modalities, there is no break between the induction and maintenance regimens. In some modalities, the induction regimen comprises the administration of multiple doses of anti-α4β7 antibody. <i407 al paciente.To prevent HAHA, the patient may be treated with a high starting dose, for example, at least 1.5 mg / kg, at least 2 mg / kg, at least 2.5 mg / kg, at least 3 mg / kg, at least 5 mg / kg, at least 8 mg / kg, at least 10 mg / kg, between about 5 and 25 mg / kg, between about 6 and 20 mg / kg, or between about 2 and about 6 mg / kg, or frequent starting administrations, for example, about once a week, about once every two weeks, or about once every three weeks of the standard dose when starting therapy with an anti-α4 antibody. In certain modalities, the treatment method maintains at least 30%, at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, or at least 10% of the standard dose when starting therapy with an anti-α4 antibody. at least 90% or at least 95% of patients as HAHA-negative. In other modalities, the treatment method keeps patients as HAHA-negative for at least 6 weeks, at least 10 weeks, at least 15 weeks, at least six months, at least 1.year, at least 2 years or throughout the therapy. In some modalities, patients, or at least 30%, at least 40%, or at least 50% or at least 60% of patients who develop HAHA maintain a low titer, for example, <125 of anti-c14p7 antibody. In one modality, the treatment method maintains at least 70% of patients as HAHA negative for at least 1.2 weeks after the start of therapy with an anti-c14p7 antibody. The anti-α4β7 antibody dose can be administered to an individual (e.g., a human) alone or in combination with another agent. A dose can be administered before, along with, or after the administration of the additional agent. In one modality, more than one formulation that inhibits the binding of α4β7 integrin to its ligands is administered. In this modality, one agent, for example, can be a monoclonal antibody, such as an anti-MAdCAM monoclonal antibody (e.g., anti-MAdCAM-AM-1) or anti-VCAM-1. In another modality, the additional agent inhibits leukocyte binding to the synothelial ligand via a pathway other than the one used for ligand binding. α4β7 pathway. This agent can inhibit the binding, 15 for example, of lymphocytes expressing chemokine receptor 9 (C*C motif) (CCR9) to chemokine expressed in the thymus (TECK or CCL25) or an agent that prevents the binding of LFA-1 to the intercellular adhesion molecule (ICAM).For example, an anti-TECK or anti-CCR9 antibody or a small-molecule CCR9 inhibitor, such as the inhibitors described in PCT publications WQ03 / 099773 or W004 / 046C92, or an anti-ICAM-1 antibody or an oligonucleotide that prevents ICAM expression, may be administered in addition to the formulation of the present invention. In another embodiment, an additional active ingredient (for example, an anti-inflammatory compound, such as sulfasalazine, azathioprine, methotrexate, 6-mercaptopurine, anti-inflammatories containing 5-aminosalicylic acid, another non-steroidal anti-inflammatory compound, a steroidal anti-inflammatory compound, or antibiotics commonly administered for the control of inflammatory bowel disease (for example, ciprofloxacin, metronidazole), probiotics, or another biological agent (for example, TNF-alpha antagonists) may be administered together with a formulation of the present invention. In one modality, the dose of the administered medication can be reduced over time during the treatment period with the anti-α4β7 antibody. For example, a patient treated with a spheroid (e.g., prednisone, prednisolone, budesonide) at the beginning of or prior to treatment with the α4β7 antibody will undergo a tapering regimen of spheroid doses, beginning at weeks 2 or 6 of treatment with the α4β7 antibody formulation. The spheroid dose will be reduced by approximately 25% within 4–8 weeks of initiating the taper, by approximately 50% at 8–12 weeks, and by approximately 75% at 12–16 weeks of tapering during treatment with the anti-α4β7 antibody formulation. In one aspect, at approximately 16-24 weeks of treatment with the anti-C4^7 antibody, the dose of spheroids can be eliminated. In another example, a patient being treated with an anti-inflammatory compound...such as 6-methylcaptopurine, at the beginning of or prior to treatment with the anti-α4p7 antibody formulation, would be subjected to a tapering regimen of the anti-inflammatory compound similar to the tapering regimen for the steroid dose mentioned above. In other modalities, a corticosteroid dose of >20 mg / day may be reduced by 5 mg / week to 20 mg / day for pediatric patients 40 kg or more, or to 0.5 mg / day for pediatric patients less than 40 kg. In other modalities, a corticosteroid dose of <20 mg / day may be reduced by 5 mg / week to 10 mg / day for pediatric patients 40 kg or more, or to 0.25 mg / day for pediatric patients less than 40 kg. In some modalities, between weeks 6 and 14 of treatment with the anti-a4p7 antibody, the corticosteroid can be further reduced by 5 mg / week to 10 mg / day, then by 2.5 mg / week to zero corticosteroid. The dose of anti-o4p7 antibody, for example, by intravenous infusion, can be administered to the pediatric patient in approximately 20, 25, 30, 35, 40, 60, 90, or 120 minutes. In some modalities, for a pediatric patient weighing 20 kg or more, the infusion time is between approximately 30 and 60 minutes. Administration may be slower for a pediatric patient of low weight (e.g., less than 20 kg); in some modalities, for a pediatric patient weighing less than 20 kg, the infusion time is approximately 2 hours. The dosing regimen can be optimized to induce a clinical response and clinical remission in the patient's inflammatory bowel disease. In some modalities, the pediatric patient with ulcerative colitis (UC) achieves a clinical response based on the total Mayo score at week 5, week 8, week 10, week 12, week 14, or week 22 after the start of treatment with the anti-a4p7 antibody. In some modalities, the pediatric patient with cirrhosis (CD) achieves a clinical response based on the CDAI score at week 6, week 8, week 10, week 12, week 14, or week 22 after the start of treatment with the anti-a4p7 antibody.In some modalities, the pediatric patient with UC achieves a clinical response of a reduction of 20 points or more from baseline in the PUCAI score and / or clinical remission of a PUCAI score of less than 10 at week 6, week 8, week 10, week 12, week 14, or week 22 after the start of treatment with the 3p1-α4β7 antibody. In some modalities, the pediatric patient with CD achieves a clinical response of a reduction of 15 points or more from baseline in the PCDAI score with a total PCDAI of 30 or less and / or clinical remission of a PCDAI score of 10 or less at week 6, week 8, week 10, week 12, week 14, or week 22 after the start of treatment with the anti-α4β7 antibody.In some modalities, a measure of remission of pediatric patients with CD is based on the CDAI components of abdominal pain, e.g., a score of 1 or less for the previous 7 days, stool frequency, e.g., ten or fewer stools for the previous 7 days, and an SES-CD score for endoscopy, e.g., less than 4, at least a remission of 2 points from the baseline value and no subscore greater than 1 on any individual variable. In some cases, the use of an anti-β4p7 antibody to treat a pediatric patient with IBD improves the patient's growth. For example, a patient may experience an increase in height, weight, or body mass index from baseline. In another example, as determined by the Tanner stage system, a measurement of the pediatric patient's clinical response to treatment with an anti-β4p7 antibody may be achieved at Tanner stage V (Marshall and Tanner, Aren. Dis. Clld. 44:291-303 (1969); Marshail and Tanner, Aren. Dis. Clld. 45:13-23 (1970)) at 16 years of age (female patients) or at 17 years of age (male patients). In some modalities, the use of a 3ηίί-α4β7 antibody for the treatment of a pediatric patient suffering from IBD results in mucosal healing.In some regimens, the use of a 3Pϋ-α4β7 antibody for the treatment of a pediatric patient with IBD reduces or eliminates the need for hospitalization and / or surgical resection of affected mucosal tissue, such as the colon or rectum. In some regimens, the use of an anti-T487 antibody corticosteroid for the treatment of a pediatric patient with IBD is reduced to discontinuation by week 48 of the treatment described herein. In some regimens, the use of a 3Pϋ-α4β7 antibody for the treatment of a pediatric patient with CD results in the healing of fistulas. In some regimens, the dosage regimen does not alter the CD4 / CD8 ratio in the cerebrospinal fluid of patients receiving the treatment. In some respects, a durable clinical remission can be achieved, for example, a clinical remission that is maintained through at least two, or at least three, visits with a treating physician within a period of six months to one year after the start of treatment, with an optimized dosing regimen. In some aspects, a durable clinical response can be achieved, for example, a clinical response that is maintained for at least 6 months, at least 9 months, at least one year, after the start of treatment, with an optimized de-dosing regimen. The method may further comprise measuring the patient's body weight. Body weight may be determined before treatment with the anti-ami-ct487 antibody, for example, vedoizumab, i.e., at the beginning, or it may be measured at other times during treatment, for example, when monitoring the patient's response. In one aspect, the present invention provides a method for treating IBD, for example, ulcerative colitis or Crohn's disease, in a high-weight pediatric patient with a higher dose (for example, 150 mg, 300 mg) of an anti-a4p7 antibody, for example, vedoizumab. In another aspect, the present invention provides a method for treating IBD, for example, ulcerative colitis or Crohn's disease, in a low-weight pediatric patient with a lower dose (for example, 100 mg, 200 mg) of an anti-a407 antibody, for example, vedoizumab. The pediatric patient may have had an inadequate response, loss of response, or intolerance to treatment with 5-aminosaiol or a derivative thereof, an immunomodulator, a TNF-α antagonist, a corticosteroid, or combinations thereof. The pediatric patient may not have received treatment with a TNF-α antagonist prior to the treatment described herein, for example, with an anti-O4p7 antibody. The pediatric patient may have previously received treatment with an immunomodulator or at least one corticosteroid (for example, prednisone or budesonide) for inflammatory bowel disease and had an inadequate response or a lack of response to it. An inadequate response to corticosteroids refers to signs and symptoms of persistently active disease.Despite a history of at least a 4-week induction regimen that included a dose equivalent to 30 mg of prednisone daily orally for 2 weeks or intravenously for 1 week. Loss of response to corticosteroids refers to two unsuccessful attempts to taper corticosteroids below a dose equivalent to 10 mg of prednisone daily orally. Corticosteroid intolerance includes a history of Cushing's syndrome, osteopenia / osteoporosis, hyperglycemia, insomnia, and / or infection. The pediatric patient may have had an inadequate response, loss of response, or intolerance to treatment with an immunomodulator. An immunomodulator may be, for example, oral azathioprine, 6-mercaptopurine, or methotrexate. An inadequate response to an immunomodulator refers to signs and symptoms of persistent active disease despite a history of at least one 8-week regimen of oral azathioprine (10.5 mg / kg), 6-mercaptopurine (10.75 mg / kg), or methotrexate (>12.5 mg / week). Intolerance to an immunomodulator includes, but is not limited to, nausea / vomiting, abdominal pain, pancreatitis, LFT abnormalities, lymphopenia, TPMT gene mutation, and / or infection. In one respect, the subject may have had an inadequate response, loss of response, or been intolerant to treatment with a TNF-α antagonist. A TNF-α antagonist, for example, is an agent that inhibits the biological activity of TNF-α and preferentially binds to TNF-α, such as a monoclonal antibody, for example, REMICADE (infliximab), HUMIRA (adalimumab), CIMZIA (certolizumab pegol), SIMEON (golimumab), or a circulating receptor fusion protein, such as ENBREL (etanercept). An inadequate response to a TNF-α antagonist refers to signs and symptoms of persistently active disease despite a history of at least a 4-week induction regimen of infliximab 5 mg / kg IV, 2 doses separated by at least 2 weeks; or a subcutaneous dose of 80 mg of adalimumab, followed by a 40 mg dose separated by at least two weeks. or 400 mg subcutaneously of certolizumab pegos, 2 doses separated by at least 2 weeks.Loss of response to a TNF-α antagonist refers to the recurrence of symptoms during maintenance dosing after prior clinical benefit. Intolerance to a TNF-α antagonist includes, but is not limited to, infusion-related reaction, demyelination, congestive heart failure, and / or infection. A loss of maintenance of remission, such comma as is used herein for subjects with ulcerative colitis, refers to an increase in the Mayo score of at least 3 points and a modified Baron score of at least 2. The methods described above regarding the treatment of a pediatric subject with IBD also apply to methods for treatment with an α4β7 integrin antagonist, such as an anti-α4β7 antibody, for example, vedolizumab, of a pediatric patient at risk of GvHD, a pediatric patient with GvHD, a pediatric patient with a monogenic defect with IBD-like pathology, a pediatric patient with glycogen storage disease type Ib, a pediatric patient with IL10 loss-of-function colitis and mutations in IL10 or IL11 receptors, and a pediatric patient with X-linked intraproliferative syndrome (defect in gene XI).AP), a pediatric patient with IPEX syndrome caused by mutations in the FOXP3 transcription factor, a pediatric patient with very early-onset inflammatory bowel disease (onset <6 years of age), a pediatric patient with indeterminate colitis (IBDU), and a pediatric patient with chronic granulomatous-associated colitis. Modifications to the method for treating pediatric patients with GvHD are described below. Treatment of pediatric subjects with graft-versus-host disease (GvHDi) using an α4β7 antibody In one aspect, the invention relates to a method for treating a pediatric patient at risk of developing GvHO, comprising the steps of: a. conditioning the patient's immune system to treat hematopoietic stem cells; b. administering an anti-α4β7 antibody, for example, a humanized antibody having binding specificity for human integrin α4β7, for example, with a dose of 100 mg or 200 mg for pediatric patients weighing less than 30 kg or with a dose of 150 mg or 300 mg for pediatric patients weighing 30 kg or more; c. waiting at least 12 hours; d. administering allogeneic hematopoietic cells; e. waiting thirteen days, then administering a second dose of the anti-α4β7 antibody; and f. waiting four weeks, then administering a third dose of the anti-α4β7 antibody. In another aspect, the invention relates to a method for suppressing an immune response in a pediatric cancer patient, wherein the method comprises the following steps: administering to a human patient undergoing an autogenic hematopoietic stem cell transplantation (alla-HSCT) an α4β7 antibody, for example, a humanized antibody having binding specificity for human integrin α4S7, wherein the antibody is administered to the patient according to the following dosage regimen: a. an initial dose of 100 or 200 mg for pediatric patients weighing less than 25 kg or a dose of 150 mg or 300 mg for pediatric patients weighing 30 kg or more of the antibody as an intravenous infusion the day before the alla-HSCT; b.followed by a second subsequent dose of 100 or 200 mg for pediatric patients weighing less than 30 kg or a dose of 150 mg or 300 mg for pediatric patients weighing 30 kg or more, of the antibody as an intravenous infusion about two weeks after the initial dose; c. followed by a third subsequent dose of 100 or 200 mg for pediatric patients weighing less than 30 kg or a dose of 150 mg or 300 mg for pediatric patients weighing 30 kg or more, of the antibody as an intravenous infusion about six weeks after the initial dose. In another aspect, the invention relates to a method for treating a patient suffering from GvHD, for example, acute GvHD occurring after an aiogenic hematopoietic stem cell transplant, by using an α4β7 integrin antagonist, such as an amphi-α4-p7 antibody: for example, 35 vedollzumab.In some modalities, the pediatric patient is administered an anti-o4p7 antibody, for example, a humanized antibody having binding specificity for human integrin «4β7», wherein the antibody is administered to the patient according to the following dosage regimen: a. an initial dose of 1.00 or 200 mg for pediatric patients under 30 kg, or a dose of 150 mg or. 300 mg for pediatric patients weighing 30 kg or more, followed by another dose two weeks later, a third dose six weeks after the initial dose, a fourth dose ten weeks after the initial dose, and a fifth dose fourteen weeks after the initial dose. In some regimens, following the previous GvHD-related doses, further treatment of a pediatric patient, for example, for six months to one year, with 100 or 200 mg for pediatric patients weighing less than 30 kg, or with a dose of 150 mg or 300 mg for pediatric patients weighing 3.0 kg or more, can maintain GvHD inhibition. In some regimens, maintaining GvHD inhibition can be achieved by administering subcutaneous doses of 54 mg, 108 mg, 160 mg, 165 mg, 216 mg, or 250 mg of 3IHIH4β7 antibody to the pediatric patient every 1 to 10 weeks. Pharmacokinetic and pharmacodynamic trials The concentration of the anti-α4β7 antibody, for example, vedolizumab, can be measured by any means known to those skilled in the art. In one aspect, the concentration of vedolizumab is measured by a sandwich enzyme-linked immunosorbent assay (ELISA). In another aspect, using a pharmacodynamic assay, the inhibition of the binding of MÁdCAM15 1-Fc to peripheral blood cells expressing O4β by the anti-α4β7 antibody, for example, vedolizumab, in the blood is used to measure the extent of αβ saturation by the O4β7 antibody, for example, vedolizumab. In one modality, the amount of 3πίI-α4β7 antibody, for example, in serum, is measured in a pharmacokinetic assay. An immobilized phase, such as a microtiter plate, container, or bead, is coated with a reagent that binds specifically to the anti-α4β7 antibody. The immobilized reagent is brought into contact with a patient sample, for example, serum, which may or may not contain the anti-α4β7 antibody. After incubation and washing, a complex forms with the anti-α4β7 antibody, and the coating reagent is brought into contact with a reagent that binds to the captured antibody and can be detected, for example, by using a label, such as horseradish peroxidase (HRP). The binding reagent can be an anti-human antibody, for example, a polyclonal or monoclonal antibody, that binds to the Fe portion of the anti-α4β7 antibody. The addition of an HRP substrate, such as 3,3?',.5.,5'-tetramefilbenzidi.na (TMB) can allow the accumulation of signal, such as the appearance of color, which can be measured, for example, in stereophotographic form. In some embodiments, the coating reagent is an anti-idiotypic antibody that binds specifically to the anti-α4β7 antibody, for example, its variable region or part thereof comprises one or more CDRs, such as the heavy chain CDR3, SEQ ID NO:6. The anti-idiotypic anti-α4β7 antibody for use in the assay may be specific for the integrin-binding portion of the α4β7 antibody and therefore bind to it, but may not be specific for the Fe portion of the anti-α4β7 antibody and therefore not bind to the Fe portion of the anti-α4β7 antibody. The anti-α4β7 anti-idiotypic antibody for use in the assay may be specific for a variable heavy and / or light chain region of the 3παβ7 antibody, and therefore bind to this, for example, selected from the group consisting of amino acids 20 to 140 of SEQ ID NO:1, amino acids 20 to 131 of SEQ ID NO:2 and amino acids 21 to 132 of SEQ ID NO:3.The anti-idiotypic anti-a4p7 antibody for use in the assay can be specific for and therefore bind to an antigen-binding fragment of the anti-a4p7 antibody. The anti-idiotypic antibody can be isolated by an immunization process using the anti-a4p7 antibody or an o4β7 integrin-binding portion thereof, such as an antibody fragment comprising one or more CDRs, and used as an isolate or produced by a recombinant method. In some embodiments, the anti-idiotypic anti-a4β7 antibody is produced against an immunogen comprising the heavy chain CDR3, SEQ ID NO:6.In other embodiments, the anti-idiotypic anti-O437 antibody is produced against an immunogen comprising a variable heavy and / or light chain region of the anti-O4p7 antibody, for example, selected from the group consisting of amino acids 20 to 140 of SEQ ID NO:1, amino acids 20 to 131 of SEQ ID NO:2, and amino acids 21 to 132 of SEQ ID NO:3. In some embodiments, the anti-idiotypic antibody is a monoclonal antibody. In some embodiments, the scFv fragment of the anti-idiotypic antibody is used in the assay. In other embodiments, the intact anti-idiotypic antibody is used in the assay. The generation of an anti-idiotypic anti-q4p7 antibody can proceed by the following general methods. A suitable animal (e.g., mouse, rat, rabbit, or sheep) can be immunized with a protein, e.g., anti-q4p7 antibody or an α4β7 integrin-binding portion thereof, or a fusion protein comprising said portion, with the immunogen prepared for injection in a manner to induce a response, e.g., with an adjuvant, e.g., Freund's complete adjuvant. Other suitable adjuvants include TITERMAX GOLD® adjuvant (CYTRX Corporation, Los Angeles, CA) and alum. Small peptide immunogens, such as a fragment comprising a CDR, such as CDR3, of the heavy chain, can be bound to a larger molecule, such as California limpet hemocyanin. Mice can be injected in a number of ways, e.g., via injection. subcutaneous, intravenous, or intramuscular at a number of sites, for example, in the peritoneum (ipThe base of the tail or a paw pad, or a combination of sites, for example, i and ia at the base of the tail, can be used for injection. Booster injections may contain the same or a different immunogen and may additionally include an adjuvant, for example, Freund's incomplete adjuvant. In general, when a monodonal antibody is desired, a hybridoma is produced by fusing a suitable cell from an immortal cell line (for example, a myeoma cell line, such as SP2 / Q, P3X63Ag8.653, or a heteromyeloma) with antibody-producing cells. The antibody-producing cells can be obtained from peripheral blood or, preferably, lymph nodes or the spleen of animals immunized with the antigen of interest.Antibody-producing cells can be produced by the use of suitable methods, e.g., fusion of a human antibody-producing cell and a heteromyeloma or trioma, or immortalization of a human B lymphocyte activated by means of Epate Barr virus infection (See, e.g., U.S. Patent No. 6,197,582 (Trakht); Niedbala et al., Hybridomas, 17:299-304 (1998); Zanella et al., J Immunol Methods. 156:205-215 (1992); Gustafeson et al., Ham Antibodfes Hybridomas, 2:26-32 (1991).) Immortalized or fused antibody-producing cells (hybridomas) can be isolated by the use of selective culture conditions and populated by dilution limitation. Cells that produce antibodies with desired specificity can be identified by using a suitable assay (e.g., ELISA with an immunogen immobilized in the myotitudinal well). The amphi-e4p7 antibody or the anti-idiolipic anti-a4p7 antibody can be produced by expressing the nucleic acid sequences encoding each strand in living cells, e.g., cultured cells. A variety of host expression vector systems can also be used to express the antibody molecules of the invention. Such host expression systems represent vehicles by which the coding sequences of interest can be produced and subsequently purified, but they also represent cells that can express an amphi-a4p7 antibody in situ when transformed or transfected with the appropriate nucleotide coding sequences. These include, but are not limited to, microorganisms such as bacteria (e.g., E. cdi, B. subtilis) transformed with recombinant bacteriophage DNA expression vectors.Piasmid or cosmid DNA AONs containing antibody-coding sequences; yeast (e.g., Saccharomyces, Pichia) transformed with recombinant yeast expression vectors containing antibody-coding sequences; insect cell systems infected with recombinant virus expression vectors (e.g., baculovirus) containing antibody-coding sequences; plant cell systems infected with recombinant virus expression vectors (e.g., cauliflower mosaic virus, CaMV; tobacco mosaic virus, TMV) or transformed with recombinant piasmid expression vectors (e.g., Ti piasmid) containing antibody-coding sequences; or mammalian cell systems (e.g., COS, CHO, BHK, 293, 3T3, NSO cells) hosting recombinant expression constructs containing promoters derived from the mammalian cell genome (e.g.,metalothionein promoter). or of mammalian viruses (e.g., the late promoter of adenylate; the 7.5K promoter of vaccinia virus). For example, mammalian cells, such as Chinese hamster ovary (CHO) cells, together with a vector, such as the major intermediate early gene promoter element of human cytomegalovirus, form an efficient expression system for antibodies (Foecking et al., Gene 45.101 (1986); Cockett et al., Bio / Technology 8:2 (1990)). In bacterial systems, a number of expression vectors can be advantageously selected, depending on the intended use of the antibody molecule being expressed. For example, when a large quantity of such a protein is required for the generation of pharmaceutical compositions of an antibody molecule, vectors that direct the expression of high levels of readily purified fusion protein products may be desirable. Such vectors include, but are not limited to, the pUR278 expression vector from E. ccli. (Ruther et al, EMBQ J. 35 2:1791 (1983)), in which the antibody coding sequence can be individually ligated to the vector in the same frame with the lac Z coding line to produce a fusion protein; pIN vectors (Inouye & Inouye, Nuteíc. Acids Res. 13:3101-3109 (1985); Van Heeke & Schuster, J. Bioí. Ctiem.24:5503-5509 (1989)); and similar ones—, pGEX vectors can also be used to express foreign polypeptides as fusion proteins with glutathione S-transferase (GST). In general, such fusion proteins are soluble and can be readily purified from cells by adsorption and binding to an agarose-glutathione microsphere array, followed by effusion in the presence of free glutathione. pGEX vectors are designed to include thrombin or factor Xa protease cleavage sites so that the cloned target gene product can be released from the GST moiety. In an insect system, the nuclear polyhedrosis virus Adographa caiifomica (AcNPV) is used as a vector to express foreign genes. The virus grows in Spodoptera frugiperda cells.The antibody coding sequence can be individually cloned into non-essential regions (e.g., the polyhedrin gene) of the virus and placed under the control of an AcMPV 10 promoter (e.g., the polyhedrin promoter). In other embodiments, the coating reagent is an antibody ligand, such as MAdCAM or an α4β7 integrin-binding fragment thereof, or a fusion protein comprising an ο4β7 integrin-binding fragment of MAdCAM fused to a protein other than MAdCAM, such as an immunoglobulin G constant domain. Examples of MAdCAM reagents and fusion proteins are described in PCT publication WO9624673 and in U.S. Patent No. 7,803,904, the full texts of which are incorporated herein by reference. HAHA Essay Activity against the human 3ηϋ-α4β7 antibody (HAHA) can be determined by detecting and / or measuring anti-drug antibodies (ADAs) or antibodies specific to the 8ηίί-α4β7 antibody (anti-vedolizumab antibodies). Several options are available, including screening and titration assays, confirmatory assays, and neutralization assays. Serum samples can be measured first in screening samples using dilutions such as 1:6 and 1:50. Positive samples can then be confirmed to verify their specificity, titrated, and tested for the ability to neutralize the anti-~s4p7 antibody, for example, vedolizumab activity. An evaluation assay can use a plating ELISA in which the plate is coated with the anti-α4p7 antibody. The immobilized anti-α4p7 antibody captures the ADA in the test sample, which is bound by a biotin-conjugated anti-α4p7 antibody labeled with horseradish peroxidase (HRP)-labeled streptavidin. The ADA is then detected by an enzyme substrate, such as TMB. A positive development, for example, as measured on a microplate reader, such as Spectramax, with analytical software, such as SOFTMAX Pro 3.1, 2, indicates the presence of ADA in the sample. The assay cutoff, for example, in the biotin-avidin-HRP-based plating assay, can be determined by using normal human serum samples as negative controls.The average absorbance values ​​of the 10 negative control sera can be added to 1.65 times the standard deviation of the negative controls to determine the cutoff point. Therefore, the cutoff point can allow for a false-positive rate of 5%. In the presence of vedolizumab at concentrations of 1 µg / mL, low titration responses are interfered with, becoming undetectable, although high immunogenicity levels are detectable at vedolizumab concentrations greater than 1 µg / mL. For example, while the sensitivity of a standard assay may be 0.44 ng / mL, in the presence of 0.5 µg / mL of vedolizumab, the assay sensitivity may be 180 ng / mL. For these reasons, serum samples can be taken more than 4 weeks, more than 8 weeks, more than 12 weeks, or more than 16 weeks after the final dose of the 5-3πϋ-α4β7 antibody. With a longer time period between the previous dose and sample collection, serum drug levels will be higher.They can typically be below the interference level. Another assay method uses streptavidin-coated plates, biotin-labeled anti-α4β57 antibody anchored to streptavidin-coated beads or microplates for the immobilized side of the bridge, and anti-α4β57 antibody labeled (for example, with a Suifo tag) with a heavy metal, such as ruthenium, osmium, or pentoxide, for the other side of the bridge. The bridged complex can be built up on the plate by addition steps and intermediate washes—or in solution, with both sides of the bridge in contact with the diluted serum sample, then transferred to the plate. An example of an assay using this method has a sensitivity of 3.90 ng / mL against anti-α4β57 antibody.Detection of the heavy metal-labeled bridging complex, for example, a ruthenium-15-labeled complex, by electrochemiluminescence (ECL), for example, on a Meso Scale Discovery Sector Imager 6000 (Rockville, MD), may be more sensitive than an HRP method and / or have greater tolerance to the amount of α4β7 antibody in serum. Therefore, there would be no need to wait for a delayed sample after the serum drug level decreases. In some modalities, pretreating the serum sample with acid, for example, low-pH acetic acid or glycine, to release the anti-α4β7 antibody from the patient-derived anti-α4β7 antibodies before contacting the anti-α4β7 antibodies can reduce interference from the serum drug. For example, while the standard assay sensitivity may be 3.90 ng / ml, in the presence of 5 g / ml of vedolizumab in serum, the assay sensitivity may be 10 ng / ml.In one embodiment, an assay for detecting anti-vedolizumab antibodies in a 25% serum sample from a patient comprises diluting the serum by a standard dilution factor, such as 1:0.5, 1:25, 1:50 and / or 1:125; treating with acetic acid; combining the treated diluted sample with an assay composition comprising a pH reagent, such as a high-strength TRIS buffer to neutralize the acid, a biotin-labeled vedolizumab and a ruthenium-labeled vedolizumab for a time sufficient to form a bridge with anti-vedolizumab antibodies between the two labeled versions of vedolizumab; transferring the complexes to a streptavidin-coated plate; washing the plate so that only ruthenium is present in complex with the antibody bridge.The detection of the ruthenium-labeled complex and measurement of the sample by effluent pyrimidine in the microplate reader can be achieved by adding reading solution, such as triprpropion, and applying voltage to stimulate the ruthenium label in complex with the plate by means of the antibody bridge. After the initial screening assay, samples can be further tested in a confirmatory assay using excess unlabeled anti-q4p7 antibody to demonstrate specificity. Confirmed positive samples can be further evaluated for HAHA's ability to neutralize the binding of anti-q4p7 antibody, e.g., vedolizumab, to cells. A competitive flow cytometry-based assay was designed to determine the ability of immune serum to inhibit the binding of labeled vedolizumab to a cell line expressing the integrin CUPα, RPMI8866, and detection by flow cytometry. The results may indicate categories of immunogenicity status: Negative: no HAHA-positive samples; Positive: at least one HAHA-positive sample; Transiently positive: at least one HAHA-positive sample and no consecutive HAHA-positive samples; and Persistently positive: at least two or more consecutive HAHA-positive samples. Negative patients are likely to respond to anti-a4p7 antibody and can continue to be treated with this antibody. Persistently positive patients are likely to have high clearance of anti-a407 antibody and may not respond to treatment with anti-a437 antibody. Positive patients may have high clearance of anti-a467 antibody and may not respond to anti-a4p7 antibody.Positive patients may have an additional serum sample taken 2, 3, 4, 5, or 6 weeks after the last dose of α4β7 antibody to determine whether they are persistently positive or transiently positive. Transiently positive patients are likely to respond to α4β7 antibody treatment, and their treatment may be continued. Immunogenicity levels can also be determined. Titer categories include ≤5 (low), ≤50, ≤125, >625, and >3125 (high). A patient with a high titer in a positive sample may have high clearance of the anti-a4p7 antibody and may not respond to anti-a487 antibody treatment. A patient with a low titer in a positive sample may respond to anti-a487 antibody treatment. The invention can be understood in greater detail with reference to the following three examples. However, these should not be considered as limiting the scope of the invention. All bibliography and patent references are incorporated herein by way of reference. EXAMPLES EXAMPLE 1 A randomized, double-blind, phase 2 dose-interval study involving pediatric patients (male and female, 2 to 17 years of age, inclusive) with moderate to severe active ulcerative colitis (UC) or cirrhosis will be used to evaluate the pharmacokinetics, efficacy, immunogenicity, safety, and tolerability of intravenous vedoizumab. Pediatric patients will have had an inadequate response, loss of adequate response, or intolerance to at least one of the following: corticosteroids, immunomodulators, and / or TNF-α antagonist therapy. Approximately 80 pediatric subjects will be enrolled to ensure that 40 subjects weighing 30 kg or more and 40 subjects weighing less than 30 kg are enrolled in the study, as well as a minimum of 36 subjects with UC and a minimum of 36 subjects with cirrhosis. This study includes a 4-week assessment period, followed by a 22-week double-blind treatment period (with the last dose administered at week 14) for all subjects. Eligible subjects may exit the study at week 22 and continue receiving the study drug in an open-label extension (OLE) study. Subjects who do not enter the OLE study will participate in an 18-week follow-up period beginning after their last dose of the study drug and will complete a long-term follow-up safety survey by telephone six months after their last dose. A schematic of the study design is included in Figure 1. EXAMPLE 2 A long-term, open-label, phase 2b extension study will be conducted in which five male and female pediatric subjects with UC or CD who initiated IV vedolizumab treatment in the phase 2 study described in Example 1 will be enrolled. The study will evaluate the long-term safety of vedolizumab administered by IV infusion. The study will also evaluate the effect of long-term IV vedolizumab treatment on time to major IBD-related events (hospitalization, surgery, or procedures), health-related quality of life measures, growth and development patterns, and exploratory efficacy measures. Subjects will receive vedolizumab IV every eight weeks at the dose administered at week 14 in the study described in Example 1 (i.e., subjects weighing less than 30 kg will receive 100 or 200 mg; subjects weighing 30 kg or more will receive 150 or 300 mg). Subjects who experience disease worsening while receiving the low dose (i.e., 100 or 150 mg) may have their dose increased to a high dose (i.e., 200 or 300 mg) at the investigator's discretion. After completion of the study in Example 1, subjects whose dose was increased based on lack of response should receive a dose based on their weight at the time of lack of response. Blood samples will be collected every 8 weeks to assess pharmacokinetics (PK); the presence of anti-vedolizumab antibodies (AVA) will be assessed every 16 weeks. The study will include an 18-week follow-up period (final safety visit) and a long-term follow-up safety survey by telephone, 5 months after the subject's last dose of the study drug, for all subjects, including those who discontinued the study. EXAMPLE 3 A study was conducted in monkeys to support the expected safety in humans. The 25 monkeys approximate human pediatric patients (e.g., human patients aged 2–4 years to 13 years) and, therefore, effects on human patients weighing <30 kg could be inferred from this study. The objective of the study was to evaluate the toxicokinetic profile and toxicity of vedolizumab (also known as MLN0002) when administered weekly by intravenous infusion to young cynomolgus monkeys for 13 weeks, and to assess the recovery, persistence, or evolution of any effects after the 12-week recovery period. MLN00Q2 was administered once weekly by intravenous infusion (approximately 30 minutes) to young cynomolgus monkeys (11 to 15 months of age and weighing between 1.2 and 2.1 kg at baseline) for 13 weeks in sterile water for injection as a 35 solution at 0 (control, 0.9% physiological saline), 10, 30, and 100 mg / kg (4 / sex / group). To assess the resolution of any effects, a 12-week recovery period was conducted (2 / sex / group for Q [control] and 100 mg / kg only). The parameters evaluated were as follows.• survival, clinical observations, body weights, food intake, ophthalmology, electrocardiography, clinical pathology parameters (hematology, coagulation, clinical chemistry and urinalysis), toxicokinetic parameters, primate anti-human antibodies (PAHA), T lymphocyte-dependent antibody response (TDAR), flow cytometry analysis (for lymphocyte subsets in peripheral blood, cerebrospinal fluid, pharmacodynamic markers), macroscopic necropsy findings, organ weights and histopathological findings. There were no consistent gender-related differences in serum exposure to MLN0002 after dosing on day 1 and day 85. MLN0002 could be quantified at the first time of sample collection after the end of infusion (EOi), and median Uv values ​​of 0.583 after the start of infusion (SOI), i.e., 5 minutes after EOI, were found for all groups on both day 1 and day 85. However, W values ​​in four individuals were 24.5 and 168.5 after SOI (24 and 168 hours after EOI), suggesting possible extravascular dosing in these individuals. Increasing the MLN0002 dose from 10 to 30 mg / kg resulted in approximately dose-proportional increases in MLN0002 AUC on day 1. Dose-proportionality in the increase in MLN0002 AUC on day 85 at these doses could not be determined in males due to the presence of anti-MLN0002 antibodies and was greater than dose-proportional in females (11.1-fold, n=1 female). All animals (n=4 / sex) in the 10 mg / kg dose group and 3 animals in the 30 mg / kg dose group (n=4 / sex) were positive for anti-MLN0002 antibodies at 168 hours post-infusion (EOI) on day 85.The detection of antibodies in these animals was associated with a marked decrease in MLN0002 exposure at the 10 mg / kg dose and in two of the three animals that tested positive for anti-MLN0002 antibodies at 30 mg / kg; however, the exposure in the third antibody-positive animal at 30 mg / kg was similar to the exposure in the remaining animals in the antibody-negative group. Increasing the MLN0002 dose from 30 to 100 mg / kg resulted in approximately dose-proportional (males) or greater than dose-proportional (females) increases in the AUC of MLN0002 on day 1 and day 85, respectively. Table 1 Summary of toxicokinetic parameters of MLN002 in serum after intravenous infusion every week by half to young cynomolgus monkeys for 13 weeks (excluding animals with exposure affected by anti-MLN0002 antibodies) Dose T . 3 < max Cmax AUC«>f88hr (mg / kg) (hr) (pg / mL) (hr*pg / mL) Day 1: Male Female Male Female Male Female 0 N / CN / C <lloq <lloq 10 0,583 253 286 22 270 300 30 0.583 712 675 66 100 56 600 2460 3370 209 000259 000 día 85”: macho hembra 0 n c 7,87 41,3 nd 1090 754 114 51 700 3030 3710 311 000362 000N / C = not applicable; <lloq = por debajo del limíte de cuantificación; auco-iwr="área" bajo ia curva concentración plasma y tiempo desde ei momento 0 a 168 horas; cmax="máximo" observado: nd ~ no se determinó; tn»="tiempo" hasta alcanzar 0«^.3 Time-dependent parameters were calculated using nominal post-infusion (SOI) times. b Values ​​exclude animals that were positive for the anti-drug antibody. All animals survived to the end of the study. There were no clinical observations related to the study article, nor effects on body weight, food consumption, ophthalmology, electrocardiology, clinical pathology parameters (hematology, coagulation, clinical chemistry and urinalysis), T-cell-dependent antibody response (TOAR), flow cytometry analysis (peripheral blood and cerebrospinal fluid), macroscopic and microscopic findings, or organ weight. At 10, 30 and 180 mg / kg, the occupation of o4;37 receptors in B lymphocytes and CD4+ memory T lymphocytes in the presence of MLN0002 was demonstrated during the dosing phase, as there was no reduction in the median fluorescence intensity values ​​of labeled MLN0002 compared to the pre-dose values ​​of the group and the control group. In conclusion, administration of MLN00Q2 once every other week by intravenous infusion was well tolerated in young cynomolgus monkeys at levels of 10, 30, and 100 mg / kg. There were no signs of toxicity at levels up to 100 mg / kg. Therefore, 100 mg / kg was considered the no-adverse-effect level (NOAEL) in this study. The serum AUCoi68hr and Cmax associated with NOAEL were 311,008 and 362,000 pg / mL in males and 3710 pg / mL in females. LIST OF SEQUENCES SEQ ID NO'I Met Gly Trp Ser Cys lie He Leu Phe Leu Val Ate Thr Ala Thr Gly 15 1015 Val His Ser Gln Val Gln Leu Val Gln Ser Gly Ate Glu Val Lys Lys 20 2530 Pro Gly Ala Ser Val Lys Val Ser Cys Lys Gly Ser Gly Tyr Thr Phe 35 4045 Thr Ser Tyr Trp Met His Trp Val Arg Gln Ala Pro Gly Gln Arg Leu 50 5560 Glu Trp He Gly Glu lie Asp Pro Ser Glu Ser Asn Thr Asn Tyr Asn 70 7580 Gln Lys Phe Lys Gly Arg Val Thr Leu Thr Val Asp He Ser Ala Ser 85 9095 Thr Ala Tyr Met Glu Leu Ser Ser Leu Arg Ser Glu Asp Thr Ala Val 100 105110 Tyr Tyr Cys Ala Arg Gly Gly Tyr Asp Gly Trp Asp Tyr Ala lie Asp 115 120125 Tyr Trp Gly Gln Gly Thr Leu Val Thr Val Ser Ser Ala Ser Thr Lys 130 135140 Gly Pro Ser Val Phe Pro Leu Ala Pro Ser Ser Lys Ser Thr Ser Gly 145 150 155160 Gly Thr Ala Ala Leu Gly Cys Leu Val Lys Asp Tyr Phe Pro Glu Pro 165 170175 Val Thr Val Ser Trp Asn Ser Gly Ala Leu Thr Ser Gly Val His Thr 180 185190 Phe Pro Ala Val Leu Gln Ser Ser Gly Leu Tyr Ser Leu Ser Ser Val 195 200205 Val Thr Val Pro Ser Ser Ser Leu Gly Thr Gln Thr Tyr He Cys Asn 210 215220 Val Asn His Lys Pro Ser Asn Thr Lys Val Asp Lys Lys Val Glu Pro 225 230 235240 Lys Ser Cys Asp Lys Thr His Thr Cys Pro Pro Cys Pro Ala Pro Glu 245 250255 Leu Ala Gly Ala Pro Ser Val Phe Leu Phe Pro Pro Lys Pro Lys Asp 260 265270 Thr Leu Met lie Ser Arg Thr Pro Glu Val Thr Cys Val Val Val Asp 275 280285 Val Ser His Glu Asp Pro Glu Val Lys Phe Asn Trp Tyr Val Asp Gly 5 290 295 300 Val Glu Val His Asn Ala Lys Thr Lys Pro Arg Glu Glu Gln Tyr Asn 305 310 315 320 Ser Thr Tyr Arg Val Val Ser Val Leu Thr Val Leu His Gln Asp Trp 325 330 335 Leu Asn Gly Lys Glu Tyr Lys Cys Lys Val Ser Asn Lys Ala Leu Pro 340 345 350 Ala Pro He Glu Lys Thr lie Ser Lys Ala Lys Giy Gln Pro Arg Glu 355 360 365 10 Pro Gln Val Tyr Thr Leu Pro Pro Ser Arg Asp Glu Leu Thr Lys Asn 370 375 380 Gln Val Ser Leu Thr Cys Leu Val Lys Giy Phe Tyr Pro Ser Asp lie 385 390 395 400 Ala Val Glu Trp Glu Ser Asn Gly Gln Pro Glu Asn Asn Tyr Lys Thr 15 405 410 415 Thr Pro Pro Val Leu Asp Ser Asp Gly Ser Phe Phe Leu Tyr Ser Lys 420 425 430 Leu Thr Val Asp Lys Ser Arg Trp Gln Gln Giy Asn Val Phe Ser Cys 435 440 445 20 Ser Val Met His Glu Ala Leu His Asn His Tyr Thr Gln Lys Ser Leu 450 455 460 Ser Leu Ser Pro Gly Lys 465 470 25 SEQ ID NO:2 Met Gly Trp Ser Cys ile ile Leu Phe Leu Val Ala Thr Ala Thr Gly 1 5 10 15 Val His Ser Asp Val Val Met Thr Gln Ser Pro Leu Ser Leu Pro Val 20 25 30 30 Thr Pro GiyGlu Pro Ala Ser He Ser Cys Arg Ser Ser Gln Ser Leu 35 40 45 Ala Lys Ser Tyr Gly Asn Thr Tyr Leu Ser Trp Tyr Leu Gln Lys Pro 50 55 60 Gly Gln Ser Pro Gln Leu Leu He Tyr Gly lie Ser Ser Ass Arg Phe Ser 35 65 70 75 80 Gly Val Pro Asp Arg Phe Ser Gly Ser Giy Ser Giy Thr Asp Phe Thr 85 90 95 Leu Lys lie Ser Arg Val Glu Ala Glu Asp Val Gly Val Tyr Tyr Cys 100 105 110 Leu Gly Gly Thr His Gln Pro Tyr Thr Phe Gly Gln Giy Thr Lys Val 115 120 125 Gilí He Lys Arg Thr Val Ala Ala Pro Ser Val Phe lie Phe Pro Pro 130 135 140 Ser Asp Glu Gln Leu Lys Ser Gly Thr Ala Ser Val Val Cys Leu Leu 145 150 155160 Asn Asn Phe Tyr Pro Arg Glu Ala Lys Val Gln Trp Lys Val Asp Asn 165 170175 Ala Leu Glr¡ Ser Giy Asn Ser Gln Glu Ser Val Thr Glu Gln Asp Ser 180 185190 Lys Asp Ser Thr Tyr Ser Leu Ser Ser Thr Leu Thr Leu Ser Lys Ala 195 200205 Asp Tyr Glu Lys His Lys Val Tyr Ala Gys Glu Val Thr His Gln Gly 210 215220 Leu Ser Ser Pro Val Thr Lys Ser Phe Asn Arg Gly Glu Cys 225 230235 SEQ ID NO:3 Asp Val Val Msi Thr Gln Ser Pro Leu Ser Leu Pro Val Thr Pro Gly 1 5 1015 Glu Pro Ala Ser He Ser Cys Arg Ser Ser Gln Ser Leu Ala Lys Ser 20 2530 Tyr Gly Asn Thr Tyr Leu Ser Trp Tyr Leu Gln Lys Pro Gly Gln Ser 35 4045 Pro Gln Leu Leu lie Tyr Gly lie Ser Asn Arg Phe Ser Gly Val Pro 50 5560 Asp Arg Phe Ser Gly Ser Gly Ser Gly Thr Asp Phe Thr Leu Lys lie 65 70 7580 Ser Arg Val Glu Ala Glu Asp Val Gly Val Tyr Tyr Cys Leu Gln Giy 85 9095 Thr His Gln Pro Tyr Thr Phe Gly Gln Gly Thr Lys Val Glu He Lys 100 105110 Arg Ala Asp Ala Ala Pro Ser Val Phe lie Phe Pro Pro Ser Asp Glu 115 120125 Gln Leu Lys Ser Gly Thr Ala Ser Val Val Cys Leu Leu Asn Asn Phe 130 135140 5 Tyr Pro Arg Glu Ala Lys Va! Gln Trp Lys Val Asp Asn Ala Leu Gln 145 150 155 160 Ser Gly Asn Ser Gín Glu Ser Val Thr Glu Gln Asp Ser Lys Asp Ser 165 170 175 Thr Tyr Ser Leu Ser Ser Thr Leu Thr Leu Ser Lys Ala Asp Tyr Glu 180 185 190 Lys His Lys Val Tyr Ala Cys Glu Val Thr His Gln Gly Leu Ser Ser 195 200 205 Pro Val Thr Lys Ser Phe Asn Arg Gly Glu Cys 10 210 215 SEQ ID NO:4 Ser Tyr Trp Met His 1 5 15 SEQ ID NO:5 Glu lie Asp Pro Ser Glu Ser Asn Thr Asn Tyr Asn Gln Lys Phe Lys 1 5 10 15 Gly 20 SEQ ID NO:6 Gly Gly Tyr Asp Gly Trp Asp Tyr Ala Be Asp Tyr 1 5 10 25 30 SEQ ID NO: 7 Arg Ser Ser Gln Ser Leu Ala Lys Ser Tyr Giy Asn Thr Tyr Leu Ser 1 S 10 15 SEQ ID NO:8 Gly lie Ser Asn Arg Phe Ser 1 5 SEQ ID NO:9 Leu Gin Gly Thr His Gln Pro Tyr Thr 35 1 5 SEQ ID NO: 10 Asp Be Val Met Thr Gln Ser Pro Leu Ser Leu Pro Val Thr Pro Gly 5 1015 Glu Pro Ala Ser He Ser Cys Arg Ser SerGin Ser Leu Leu His Ser 2530 Asn Gly Tyr Asn Tyr Leu Asp Trp Tyr Leu Gln Lys Pro Gly Gln Ser 4045 Pro Gln Leu Leu He Tyr Leu Giy Ser Asn Arg Ala Ser Gly Val Pro 5560 Asp Arg Phe Ser Gly Ser Gly Ser Giy Thr Asp Phe Thr Leu Lys He 70 7580 Ser Arg Val Glu Ala Glu Asp Val Gly Val Tyr Tyr Cys Met Gln Ala 9095 Leu Gln Thr Pro Gln Thr Phe Gly Gln Giy Lys Val Glu lie Lys 100 105110 SEQ ID NO:11 Gln Val Gln. Leu Val Gln Ser Gly Ala Glu Val Lys Lys Pro Gly Ala 5 1015 Ser Val Lys Val Ser Cys Lys Ala Ser Gly Tyr Thr Phe Thr Ser Tyr 2530 Ala Met His Trp Val Arg Gln Ala Pro Gly Gln Arg Leu Glu Trp Met 4045 Gly Trp He Asn Ala Gly Asn Gly Asn Thr Lys. Tyr Ser Gln Lys Phe 556Θ Gln Gly Arg Val Thr He Thr Arg Asp Thr Ser Ala Ser Thr Ala Tyr 70 7580 Met Glu Leu Ser Ser Leu Arg Ser Glu Asp Thr Ala Val Tyr Tyr Cys 9095 Ala Arg Gly Gly Tyr Tyr Gly Ser Giy Ser Asn Tyr Trp Gly Gin Gly 100 105110 Thr Leu Val Thr Val Ser Ser< / lloq> < / lloq>

Claims

1. A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having inflammatory bowel disease (IBD): of a first 200 mg dose of an antibody having binding specificity for human integrin α4β7, a second 200 mg dose of the antibody two weeks after the first dose, and a third 200 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO: 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO:

2.

2. The method of claim 1, further comprising a fourth dose of 200 mg at 14 weeks after the first dose.

3. The method of claim 1 or 2, further comprising subsequent doses of 200 mg every eight weeks thereafter. 15 4. The method of any of the preceding claims, wherein the antibody heavy chain comprises amino acids 20 to 470 of SEQ ID NO1 and the antibody light chain comprises amino acids 20 to 238 of SEQ ID NQ:2, 5. The method of any of the preceding claims, wherein each dose is administered intravenously as an infusion over approximately 120 minutes. 20 6. The method of any of the preceding claims, wherein the pediatric patient weighs less than 30 kg.

7. The method of any of claims 1-5, wherein the pediatric patient weighs between 10 kg and 30 kg.

8. The method of any of the preceding claims, wherein 25 inflammatory bowel disease is moderately to severely active Crohn's disease.

9. The method of any of claims 1-7, wherein the inflammatory bowel disease is moderately to severely active ulcerative colitis, 10. The method of any of the preceding claims, wherein the pediatric patient may have had inadequate response, loss of response, or was intolerant to a 30 TNFα antagonist.

11. The method of any of claims 1-9, wherein the pediatric patient had an inadequate response or loss of response to a corticosteroid.

12. The method of any of claims 1-9, wherein the pediatric patient had an inadequate response or loss of response to an immunomodulator. 35 13. The method of any of the preceding claims, wherein a clinical response is achieved as measured at week 14.

14. The method of any of the preceding claims, wherein the pediatric patient achieves remission of inflammatory bowel disease.

15. The method of any of the preceding claims, wherein the dose is obtained from a container manufactured to administer 20 mg of the antibody.

16. A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of: a first 100 mg dose of an antibody having binding specificity for human integrin ο4β7, a second 100 mg dose of the antibody two weeks after the first dose, and a third 100 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO: 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO:

2.

17. The method of claim 16, further comprising a fourth dose of 200 mg at 14 weeks after the first dose.

18. The method of claim 17, further comprising a fifth and subsequent doses of 200 mg every eight weeks after the fourth dose.

19. The method of any of the preceding claims, wherein the heavy chain of the antibody comprises amino acids 20 to 470 of SEQ ID NO:1 and the light chain of the antibody comprises amino acids 20 to 238 of SEQ ID NO:

2.

20. The method of any of the preceding claims, wherein each dose is administered intravenously as an infusion over approximately 120 minutes.

21. The method of any of claims 16-20, wherein the pediatric patient weighs less than 30 kg.

22. The method of any of claims 16-20, wherein the pediatric patient weighs between 10 kg and 30 kg.

23. The method of any of claims 16-22; wherein inflammatory bowel disease is moderately to severely active Crohn's disease.

24. The method of any of claims 16-22, wherein the inflammatory bowel disease is moderately to severely active ulcerative colitis.

25. The method of any of claims 16-24, wherein the pediatric patient may have had an inadequate response, loss of response, or was intolerant to a TNFα antagonist.

25.

26. The method of any of claims 16-24, wherein the pediatric patient had an inadequate response or loss of response even to corticosteroid.

26.

27. The method of any of claims 16-24, wherein the pediatric patient had an inadequate response or loss of response to an immunomodulator, 27.

28. The method of any of claims 16-27, wherein a clinical response is achieved as measured at week 14, 28.

29. The method of any of claims 16-27, wherein the pediatric patient achieves remission of inflammatory bowel disease, 29.

30. The method of any of claims 16-29, wherein the dose is obtained from a container manufactured to administer 100 mg of the antibody.

30.

31. A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD: of a first 150 mg dose of an antibody having de-binding specificity for human integrin ο4β7, a second 150 mg dose of the antibody two weeks after the first dose, and a third 150 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO. 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID MO:

2.

31.

32. The method of claim 31, further comprising a fourth dose of 150 mg 1Q at 14 weeks after the first dose.

32.

33. The method of claim 31, further comprising a fourth dose of 300 mg at 14 weeks after the first dose.

33.

34. The method of claim 32, further comprising a fifth and subsequent doses of ISO mg every eight weeks after the fourth dose. 15 35. The method of claim 33, further comprising a fifth and subsequent doses of 300 mg every eight weeks after the fourth dose.

36. The method of any of claims 31-35, wherein the antibody heavy chain comprises amino acids 20 to 470 of SEQ ID NO:1 and the antibody light chain comprises amino acids 20 to 238 of SEQ ID NO:

2. 20 37. The method of any of claims 31-36, wherein each dose is administered intravenously as an infusion over approximately 30 minutes.

38. The method of any of claims 31-37, wherein the pediatric patient weighs 30 kg or more.

39. The method of any of claims 31-37, wherein the pediatric patient weighs between 10 kg and 30 kg. 40.

41. The method of any of claims 31-39, wherein the inflammatory bowel disease is moderately to severely active Crohn's disease.

42. The method of any of claims 31-41, wherein the inflammatory bowel disease is moderately to severely active ulcerative colitis.

43. The method of any of claims 31-41, wherein the pediatric patient may have had an inadequate response, loss of response, or intolerance to a TNFα antagonist.

44. The method of any of claims 31-41, wherein the pediatric patient had an inadequate response or loss of response to a co-steroid.

34. The method of any of claims 31-42, wherein the pediatric patient had an inadequate response or loss of response to an immunomodulator.

45. The method of any of claims 31-44, wherein a clinical response is achieved as measured at week 14.

46. The method of any of claims 31-45, wherein the pediatric patient achieves remission of inflammatory bowel disease.

47. The method of any of claims 31-46, wherein the dose is obtained from a container manufactured to administer 150 mg of the antibody. 48.A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of: a first 300 mg dose of an antibody having binding specificity for human integrin α4β7, a second 300 mg dose of the antibody two weeks after the first dose, and a third 300 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO. 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO.

2.

49. The method of claim 48, further comprising a fourth 300 mg dose at 14 weeks after the first dose.

50. The method of claim 49, further comprising a fifth and subsequent 15 doses of 300 mg every eight weeks after the fourth dose. 51.The method of any of claims 48-50, wherein the antibody heavy chain comprises amino acids 20 to 470 of SEQ ID NO:2 and the antibody light chain comprises amino acids 20 to 238 of SEQ ID NO:

2.

52. The method of any of claims 48-51, wherein each dose is administered intravenously as an infusion over approximately 30 minutes.

53. The method of any of claims 48-52, wherein the pediatric patient weighs 30 kg or more.

54. The method of any of claims 48-53, wherein the inflammatory bowel disease is moderately to severely active Crohn's disease.

55. The method of any of claims 48-53, wherein the inflammatory bowel disease is moderately to severely active ulcerative colitis. 56.The method of any of claims 48-55, wherein the pediatric patient had an inadequate response, loss of response, or was intolerant to a TNF antagonist.

57. The method of any of claims 48-55, wherein the pediatric patient had an inadequate response or loss of response to a corticosteroid.

58. The method of any of claims 48-55, wherein the pediatric patient had an inadequate response or loss of response to an immunomodulator.

59. The method of any of claims 48-58, wherein a clinical response is achieved as measured at week 14.

60. The method of any of claims 48-59, wherein the pediatric patient achieves remission of inflammatory bowel disease. 61.A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of a first 100 mg dose of an antibody having binding specificity for human integrin α4β7, a second 100 mg dose of the antibody two weeks after the first dose, and a third 100 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain CDR1 CDR3 heavy chain: CDR1 CDR2 CDR3 SEQ ID NO:7 CDR2 SEQ ID NO:8 and SEQ ID NO:9; and SEQ ID NO:4 SEQ ID NO:5 and SEQ ID NO:

6. 62.A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of: a first 200 mg dose of an antibody having binding specificity for human integrin α4β7, a second 200 mg dose of the antibody two weeks after the first dose, and a third 200 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CORs: light chain: CDR1 SEQ ID NO:7, CDR2 SEQ ID NO:8, and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5, and CDR3 SEQ ID NO:6.

63. A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD: of a first dose of 150 mg of an antibody having binding specificity for human integrin α4β7, a second dose of 150 mg of the antibody two weeks after the first dose, and a third dose of 150 mg of the antibody six weeks after the first dose, wherein the antibody comprises a non-human antigen-binding region. less a part of an antibody of human origin, wherein the antibody has a binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO:7 CDR2 SEQ ID NQ.S and CDR3 SEQ ID NO.9, and heavy chain: CDR1 SEQ ID NO:4 CDR2 SEQ ID NQ:5 and CDR3 SEQ ID NO S. 64.A method for treating inflammatory bowel disease in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD: of a first 300 mg dose of an antibody having binding specificity for human α4β7 integrin, a second 300 mg dose of the antibody two weeks after the first dose, and a third 300 mg dose of the antibody six weeks after the first dose, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex. wherein the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO:7, CDR2 SEQ ID NO:8, and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5, and CDR3 SEQ ID NO:

6. 65.The method of any one of claims 61 to 64, wherein subsequent doses of the antibody are administered subcutaneously.

66. The method of claim 65, wherein each subcutaneous dose is 108 mg of antibody.

67. The method of claim 65 or 66, wherein the subcutaneous dose is administered every two or four weeks to a pediatric patient weighing 30 kg or more.

68. The method of claim 65 or 66, wherein the subcutaneous dose is administered every three weeks, every four weeks, every five weeks, every six weeks, every seven weeks, every eight weeks, every nine weeks, or every ten weeks to a pediatric patient weighing between 10 kg and 30 kg. 69.A method for treating inflammatory bowel disease (IBD) in a pediatric patient, comprising the intravenous administration to a pediatric patient having IBD of: a first 200 mg dose of an antibody having binding specificity for human integrin α4β7, a second 200 mg dose of the antibody two weeks after the first dose, and subcutaneous administration of a third 108 mg dose of the antibody six weeks after the first dose and subsequent 108 mg doses of the antibody every two, three, or four weeks thereafter, wherein the antibody comprises a non-human antigen-binding region and at least a portion of a human antibody, wherein the antibody has binding specificity for the α4β7 complex, wherein the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO:7 CDR.2 SEQ ID NO:8 and CDR3 SEQ ID N0:9; and heavy chain: CDR 1 SEQ ID NO:4 CDR2 SEQ ID NO:5 and CDR3 SEQ ID NO 6.

70. A method for treating a pediatric cancer patient undergoing allogeneic hematopoietic stem cell transplantation (allio-HSCT), comprising intravenously administering to a pediatric patient the day before allo-HSCT a first dose of 200 mg of an antibody having binding specificity for human α4β7 integrin, a second dose of 200 mg of the antibody two weeks after the first dose, and subcutaneously administering a third dose of 108 mg of the antibody six weeks after the first dose and subsequent doses of 108 mg of the antibody every two, three, or four weeks thereafter, wherein the antibody comprises an antigen-binding region of non-human origin and at least a portion of an antibody of human origin, wherein the antibody has binding specificity for the α4β7 complex.where the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO:7, CDR2 SEQ ID NO:8, and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5, and CDR3 SEQ ID NO:

6.

71. A method for treating a pediatric patient with a monogenic defect with IBD-like pathology, comprising the intravenous administration to the pediatric patient of: a first 200 mg dose of an antibody having binding specificity for human α4β7 integrin, a second 200 mg dose of the antibody two weeks after the first dose, and a third 200 mg dose of the antibody six weeks after the first dose, where the antibody comprises a binding region to antigen of non-human origin and at least a part of-a human-origin antibody, wherein the antibody has a binding specificity for the α4β7 complex.wherein the antigen-binding region comprises the following CDRs: light chain: CDR1 SEQ ID NO:7, CDR2 SEQ ID NO:8, and CDR3 SEQ ID NO:9; and heavy chain: CDR1 SEQ ID NO:4, CDR2 SEQ ID NO:5, and CDR3 SEQ ID NO:

6. A vial manufactured for administering 200 mg of an anti-a4p7 antibody for the treatment of a pediatric patient.

73. The method of claim 71, wherein the monogenic defect—with IBD-like pathology—is selected from the group consisting of glycogen storage disease type 1b, IL10 loss of function and mutations in IL10 or IL10 receptors, X-linked lymphoproliferative syndrome, IPEX syndrome caused by mutations in the FOX-P3 transcription factor, and chronic granulomatous disease.

74. The method of claim 71 or 73, further comprising a subsequent dose of 5,200 mg every eight weeks thereafter. 75.The method of claim 71 or 73, further comprising a subsequent dose of 200 mg until the pediatric patient weighs 30 kg or more.

76. The method of any one of claims 1-4, 16-19, 61-63, 71, 73, and 74, further comprising increasing the dose to 300 mg after the pediatric patient weighs 30 kg or more.

77. The method of any one of claims 61-4, 69, and 71, wherein the antibody is a humanized antibody.

78. The method of claim 77, wherein the humanized antibody comprises a heavy chain variable region sequence of amino acids 20 to 140 of SEQ ID NO. 1 and a light chain variable region sequence of amino acids 20 to 131 of SEQ ID NO. 2.