541 results about "Autoantibody production" patented technology

Multivalent, multispecific molecules having at least one specificity for a pathogen and at least one specificity for the HLA class II invariant chain (Ii) are administered to induce clearance of the pathogen. In addition to pathogens, clearance of therapeutic or diagnostic agents, autoantibodies, anti-graft antibodies, and other undesirable compounds may be induced using the multivalent, multispecific molecules.

Compositions and methods are provided for prognostic classification of autoimmune disease patients into subtypes, which subtypes are informative of the patient's need for therapy and responsiveness to a therapy of interest. The patterns of circulating blood levels of serum autoantibodies and / or cytokines provides for a signature pattern that can identify patients likely to benefit from therapeutic intervention as well as discriminate patients that have a high probability of responsiveness to a therapy from those that have a low probability of responsiveness. Additionally, serum autoantibody and / or cytokine signature patterns can be utilized to monitor responses to therapy. Assessment of this signature pattern of autoantibodies and / or cytokines in a patient thus allows improved methods of care. In one embodiment of the invention, the autoimmune disease is rheumatoid arthritis.

The present invention relates to methods and compositions for use in treatment of patients with autoantibody positive disease. In a specific embodiment, the present invention relates to a method of treating a patient that has an ANA titer of 1:80 or greater and / or greater than or equal to 30 IU / ml of anti-dsDNA antibodies in his / her blood plasma or serum comprising administering a therapeutically effective amount of an immunomodulatory agent, such as an antagonist of Neutrokine-alpha. Additionally provided is a method of reducing the frequency and / or quantity of corticosteroid administration to patients. In preferred embodiments, the patient has systemic lupus erythematosus. Methods for determining if a lupus patient is responding to medical treatment are also provided.

The invention relates, among other things, a preparation comprising Alzheimer's disease antigen (A68), as well as methods of obtaining this purified antigen, and methods of using this purified antigen, for instance, for diagnosing Alzheimer's disease and for detecting human autoantibodies to the Alzheimer disease antigen. The antigen preparation according to the invention is purified in that it is substantially free of immunoglobulin G. The invention further relates to methods of making Alzheimer disease antigens that can be used instead of or along with the A68 antigen preparation (e.g., for diagnosing AD), such as recombinant human tau, tau isolated from various species including human, and phosphorylated recombinant human tau or isolated tau, as well as A68 anti-idiotypic antibodies.

Provided herein are novel autoantibody biomarkers, and panels for detecting autoantibody biomarkers for prostate cancer, and methods and kits for detecting these biomarkers in the serum of individuals suspected of having prostate cancer.

The present invention relates to methods and compositions for use in treatment of patients with autoantibody positive disease. In a specific embodiment, the present invention relates to a method of treating a patient that has an ANA titer of 1:80 or greater and / or greater than or equal to 30 IU / ml of anti-dsDNA antibodies in his / her blood plasma or serum comprising administering a therapeutically effective amount of an immunomodulatory agent, such as an antagonist of Neutrokine-alpha. Additionally provided is a method of reducing the frequency and / or quantity of corticosteroid administration to patients. In preferred embodiments, the patient has systemic lupus erythematosus. Methods for determining if a lupus patient is responding to medical treatment are also provided.

Processes and materials are provided for the detection, diagnosis, or determination of the severity of a neurological injury or condition, including traumatic brain injury, multiple-organ injury, stroke, Alzeimer's disease, Pakinson disease and Chronic Traumatic Encephalopathy (CTE). The processes and materials include biomarkers detected or measured in a biological sample such as whole blood, serum, plasma, or CSF. Such biomarkers include Tau and GFAP proteins, their proteolytic breakdown products, brain specific or enriched micro-RNA, and brain specific or enriched protein directed autoantibodies. The processes and materials are operable to detect the presence of absence of acute, subacute or chronic brain injuries and predict outcome for the brain injury.

Biomarkers for liver diseases and method for using the same are provided. For detecting liver cirrhosis and liver cancer, the biomarkers are selected from any one of the amino acid sequences with SEQ ID NO:1 to SEQ ID NO:24 or derivatives or fragments or variants or the combination thereof or the antibodies against the amino acid sequences. Then the biomarkers are further developed into detection kits, such that by detecting the existence of autoantibodies or autoantigens in screened specimens, liver diseases are detected with higher accuracy and sensitivity.

cDNA molecules coding for GAD65 polypeptide. The invention provides cDNA molecules comprising a part of the cDNA sequence of GAD65 which encode at least one epitope for autoantibodies to GAD65. The invention also provides cloning vehicles capable of replication and expression comprising cDNA molecules coding for GAD65. The invention further provides for hosts transformed with a vehicle having a cDNA molecule coding for GAD65. In another embodiment, the invention provides for the detection of autoantibodies to GAD65 using the GAD65 polypeptides coded for by the cDNA molecules of the invention.

The invention discloses a detection kit used for detecting the serum autoantibody of mammals. The detection kit comprises an antigen protein, wherein the antigen protein is a combination of five or more out of p53, Annexin1, CAGE, NY-ESO-1, HuD, Cyclin D, PGP9.5, GBU4-5, MDM2, GAGE7, XAGE1b, SOX2, MAGE A1 and MAGE A4. The detection kit adopts a group of novel antigen combination corresponding to the autoantibody of a biomarker related to cancers, utilizes biotins to form characteristics of a polymer to envelope the antigen protein, and uses an anti-human label peptide as a standard of quantitative detection, thus increasing the detection sensibility and accuracy of the serum autoantibody, and providing an optimized detection method for using the autoantibody to carry out cancer diagnosis.

A robust, quantitative, and reproducible process and assay for diagnosis of a neurological condition in a subject is provided. With measurement of one or more autoantibodies to biomarkers in a biological fluid such as CSF or serum, the extent of neurological damage in a subject with an abnormal neurological condition is determined and subtypes thereof or tissue types subjected to damage are discerned.

The present invention relates to methods and compositions for use in treatment of patients with autoantibody positive disease. In a specific embodiment, the present invention relates to a method of treating a patient that has an ANA titer of 1:80 or greater and / or greater than or equal to 30 IU / ml of anti-dsDNA antibodies in his / her blood plasma or serum comprising administering a therapeutically effective amount of an immunomodulatory agent, such as an antagonist of Neutrokine-alpha. Additionally provided is a method of reducing the frequency and / or quantity of corticosteroid administration to patients. In preferred embodiments, the patient has systemic lupus erythematosus. Methods for determining if a lupus patient is responding to medical treatment are also provided.

The present invention relates to a method for detecting the presence of high levels of autoantibodies against protein C / activated protein C endothelial receptor (EPCR). The invention is characterised in that it comprises in vitro detection and quantification of anti-EPCR autoantibodies in a sample.

A neurodegenerative disease or condition is diagnosed in a subject by obtaining a sample of cerebral spinal fluid from the subject and assaying the sample by an assay method that detects the presence of at least one antiphospholipid autoantibody in the sample, wherein an elevated level of at least one antiphospholipid autoantibody in the sample of cerebral spinal fluid correlates with a neurodegenerative disease or condition in the subject. The neurodegenerative disease or condition may also be diagnosed by assaying a sample of cerebral spinal fluid to detect nitrosylated antibodies, wherein an elevated level of nitrosylated antibodies correlates with a neurodegenerative disease or condition in said subject. A neurodegenerative disease or condition is also detected or diagnosed by assaying a first sample of cerebral spinal fluid from the subject to determine a level of at least one autoantibody having a selected specificity, treating a second sample of cerebral spinal fluid with an oxidizing agent and assaying the oxidized second sample to determine a level the at least autoantibody having the selected specificity, and comparing the level of the at least one autoantibody in the first sample with the level of the at least one autoantibody in the oxidized second sample, wherein a lack of increase in the level of the at least one autoantibody in the oxidized second sample as compared to the level of the at least one autoantibody in the first sample correlates with a neurodegenerative disease or condition in said subject.

The present invention relates to methods and compositions for use in treatment of patients with autoantibody positive disease. In a specific embodiment, the present invention relates to a method of treating a patient that has an ANA titer of 1:80 or greater and / or greater than or equal to 30 IU / ml of anti-dsDNA antibodies in his / her blood plasma or serum comprising administering a therapeutically effective amount of an immunomodulatory agent, such as an antagonist of Neutrokine-alpha. Additionally provided is a method of reducing the frequency and / or quantity of corticosteroid administration to patients. In preferred embodiments, the patient has systemic lupus erythematosus. Methods for determining if a lupus patient is responding to medical treatment are also provided.

The binding specificity of at least one protein suspended or dissolved in a liquid medium is reversibly altered by exposing the protein to an oxidizing agent or an electric current. A masked protein such as an autoantibody can be detected, isolated and recovered from a biological fluid by subjecting the biological fluid to an oxidizing agent or an electric current to change the binding specificity of masked proteins contained therein.

IgG and IgM autoantibody levels against phosphorylcholine in subjects with hypertension (diastolic pressure>95 mmHg) were determined at baseline in order to determine the importance of antibodies for the development of atherosclerosis. The results show that increases in intima-media thickness (IMT) at a follow-up four years after baseline were significantly less prevalent in subjects having high IgM autoantibodies to phosphorylcholine. The presence or absence of IgM autoantibodies against phosphorylcholine is thus related to an increased or decreased risk of developing ischemic cardiovascular diseases. A method to determine IgM antibodies toward phosphorylcholine is proposed in this invention to identify subjects at risk of developing ischemic cardiovascular diseases. Animal experiments show that medium to high levels of IgM antibodies can be detected in plasma after active immunization with a keyhole limpet hemocyanin (KLH)-phosphorylcholine conjugate. A pharmaceutical composition comprising a phosphorylcholine conjugate (active immunization) or a monoclonal antibody with specificity to a phosphorylcholine conjugate (passive immunization) is proposed and the use of these compositions as active or passive immunogens in the treatment or prevention of atherosclerosis.

The present invention provides a human thyroglobulin antibody magnetic separation enzymatic chemiluminescent immunoassay method, belonging to the field of immunodetection and analysis technology. Said method includes the following steps: making antigen human thyroglobulin be connected with Fe3O4 mincrosphere surface as solid phase reagent, the diameter of Fe3O4 microsphere is 0.1-5.0 microns, after the self-body antibody human thyroglobulin antibody being in the sample is trapped and two antibodies are labeled by enzyme reagent, the solid phase-antigen-antibody-enzyme-labeled two-antibody sandwiched immune complex can be formed.

The present invention relates to a novel diagnostic marker useful for the diagnosis of rheumatoid arthritis comprising the autoantibodies of mannose binding lectin protein and a process thereof.

The binding specificity of at least one plasma protein suspended or dissolved in a liquid medium is altered by exposing the protein to an oxidizing agent or an electric current sufficient to alter its binding specificity. A masked protein such as an autoantibody can be recovered from blood or blood products or extracts by oxidizing the protein to change its binding specificity.

In this invention, the inventor discloses that naturally occurring IgM anti-lymphocyte antibodies bind to chemokine and non-chemokine receptors on lymphocytes and other cells, and downmodulate certain receptors including CD4 and CD2 on T cells and CD80 and CD86 on macrophages. The inventor also discloses that such antibodies (i) inhibit HIV-1 and other viruses from infecting cells (ii) inhibits activation and proliferation of T lymphocytes (iii) inhibits cytokine and chemokine production (iv) inhibits inflammatory processes, and (v) enhances death of malignant cells. This art or invention is novel in that the antibodies described herein are “naturally occurring” i.e. develop in absence of deliberate immunization and secondly these antibodies are distinct from disease causing autoantibodies in that these naturally occurring antibodies are polyreactive with low binding affinity.

The present invention provides methods, compositions, and kits for the detection of neurodegenerative disease specific autoantibodies for the diagnosis of neurodegenerative diseases and risk for developing neurodegenerative diseases, and for the generation of patient-specific neurodegenerative disease diagnostic autoantibody profiles.

Systems and assay methods are disclosed for detecting an autoantibody in a sample. In certain instances, the systems and methods employ a mass tag releasably connected to an antigen. The tag is thereafter released for detection. A tag can be detected by mass spectrometry or in certain instances the tag is fluorescent. Methods for diagnosing a disease or disorder in a subject are also disclosed.

A blood purification sorbent for antibody removal belongs to the technical field of biomedicine, which consists of the two parts of solid-phase carrier material and a petunidin fixed on the carrier by chemical coupling. The molecular structure of the petunidin is shown as above, wherein, one atom among A, B and C is N, the others are C; n is 0-2. The blood purification sorbent can adsorb the antibody component in plasma and autoantibodies such as rheumatoid factor, antinuclear antibody, etc. in heavy load, has limited nonspecific adsorption to other plasma components such as seralbumin, etc., and also has low preparation cost and stable physicochemical property. The material can be used as adsorption filler of a blood purification device for removing the autoantibody and immune complex in the plasma.

The present invention provides assays for detecting and measuring the presence or level anti-TNFα drugs and / or the autoantibodies to anti-TNFα drugs in a sample. The present invention is useful for optimizing therapy and monitoring patients receiving anti-TNFα drug therapeutics to detect the presence or level of autoantibodies against the drug. The present invention also provides methods for selecting therapy, optimizing therapy, and / or reducing toxicity in subjects receiving anti-TNFα drugs for the treatment of TNFα-mediated disease or disorders.

Cancer cells with defects in DNA repair are highly susceptible to DNA-damaging agents, but delivery of therapeutic agents into cell nuclei can be challenging. A sub-set of autoantibodies having nucleolytic activity are capable of nuclear penetration. These antibodies can be used as therapeutic agents targeted towards DNA repair-deficient malignancies.

Provided are human alpha-synuclein-specific autoantibodies as well as fragments, derivatives and variants thereof as well as methods related thereto. Assays, kits, and solid supports related to antibodies specific for α-synuclein are also disclosed. The antibody, immunoglobulin chain(s), as well as binding fragments, derivatives and variants thereof can be used in pharmaceutical and diagnostic compositions for α-synuclein targeted immunotherapy and diagnosis, respectively.

The present invention relates to autoantibodies and the detection thereof with peptide epitopes. The invention also relates to autoantibody patterns and their correlation with biological class distinctions.

The present invention relates to methods and compositions for use in treatment of patients with autoantibody positive disease. In a specific embodiment, the present invention relates to a method of treating a patient that has an ANA titer of 1:80 or greater and / or greater than or equal to 30 IU / ml of anti-dsDNA antibodies in his / her blood plasma or serum comprising administering a therapeutically effective amount of an immunomodulatory agent, such as an antagonist of Neutrokine-alpha. Additionally provided is a method of reducing the frequency and / or quantity of corticosteroid administration to patients. In preferred embodiments, the patient has systemic lupus erythematosus. Methods for determining if a lupus patient is responding to medical treatment are also provided.

The present invention relates to methods of diagnosing peripheral neuropathies that comprise determining the titer of autoantibodies directed toward particular nervous system antigens. It also provides for substantially purified preparations of specific antigens, namely neuroprotein-1, histone H3 (NP-2), beta -tubulin (NP-3), neuroprotein-4, neuroprotein-5, NP-9 antigen, and SP neural antigen, which may be used in such diagnostic methods.