31 results about "Germinal center" patented technology

Compositions and methods for modulating the growth, proliferation, and/or differentiation of B-cells in the germinal center are disclosed, and include use of IL-15 inhibitors, antagonists, and agonists. The compositions and methods find use in treating B-cell-related disorders, including neoplasms of the B-cell lineage.

The present invention relates to novel proteins, termed INSP081, INSP082, and INSP091, herein identified as members of the Germinal Center Kinase (GCK) subfamily of the STE20 family of protein kinases, preferably as NCK-interacting kinases (NIKs) and more preferably as NIK-like embryo specific kinases (NESKs), and to the use of these and nucleic acid sequences from the encoding genes in the diagnosis, prevention, and treatment of disease.

The present invention comprises the use of follicular dendritic cells (FDCs) or FDC-like cells to generate FDC-dependent, but T cell-independent, B cell responses to T cell-dependent antigens, with antigen-specific and polyclonal antibody production in ˜48 h. In another embodiment, a germinal center (GC) lymphoid tissue equivalent (LTE) was used to generate antigen-specific IgM, followed by switching to IgG. The GC LTE model can be used in vaccine assessment. Dual forms of immunogen were used in the GC LTE and in vivo. Dual immunogens resulted in rapid, specific IgM responses and enhanced IgG responses. This vaccine design approach can be used, for example, to provide rapid IgM protection (˜24-48 h) and high-affinity IgG more quickly in people moving to areas with endemic disease, or in people with T cell insufficiencies, who can be immunized to rapidly generate protective IgM.

The present invention relates to compositions and methods of inhibiting stem cell binding to organs and tissues, including the blocking of stem cell binding to germinal centers present in lymph tissue. Disclosed are compositions and methods for regenerating germinal centers in lymphatic tissue. Included in the compositions are adjuvants, agonists to CD40, CD28 and the IL-21 receptor, and antagonist to CD20.

The invention provides an inactivated or attenuated gene functionally linked to a hotspot for somatic hypermutation. Inventive nucleic acids include inactivated genes operatively linked to immunoglobulin gene control elements. Embodiments of the invention include murine models of plasma cell disease and germinal center cell lymphoma.

The present invention provides compositions and methods for modulating cell proliferation, survival, morphology, and migration. Nucleic acids encoding proteins and proteins so encoded which are capable of modulating proliferation, survival, morphology and migration in mammalian cells are provided. Compositions and methods for the treatment of disorders related to cell proliferation, survival, morphology and migration are also provided. Prophylactics and methods for the prevention of such disorders are also provided. Also provided are compositions and methods for diagnostic and prognostic determination of such disorders. Further provided are assays for the identification of bioactive agents capable of modulating proliferation, survival, morphology and migration in mammalian cells.

The present invention describes methods to produce vaccines and antibodies, which methods including contacting follicular dendritic cells (FDC) with naïve B-cells to mimic conditions in the germinal center (CG) in vitro, including methods of enhancing antibody production in hybridoma cells and compositions comprising product of the instant methods.

Methods for identifying a therapeutic agent for treating a Germinal Center Kinase (GCK)-Like Kinase (GLK)-mediated disease are disclosed. Methods for detecting a modulation of GLK signaling by a lest compound are disclosed. Also disclosed are methods for detecting the presence and/or severity of an autoimmune disease and/or cancer.

The invention relates to a preparation method of a broad-spectrum vaccine. The preparation method comprises the following steps: combining a cross-linking agent with a pathogen; or contacting a cross-linking agent with a recombinant protein from a pathogen and allowing them to form a new protein internal covalent bond; if the pathogen is adopted, inactivation needs to be carried out, then the cross-linking agent which is not combined with the protein is removed, and if the recombinant protein from the pathogen is adopted, the cross-linking agent which is not combined with the protein is directly removed; separating the cross-linking agent modified pathogen or recombinant protein; and combining the cross-linking agent modified pathogen or recombinant protein with an adjuvant to obtain the broad-spectrum vaccine. In the maturing and hypermutation periods of B cells in a hair growth center, follicular dendritic cells present antigens with stable original ecological structures to the B cells in the hair growth center. Therefore, the B cells of the hair growth center have sufficient time to repeatedly circulate and mutate in the hair growth center, and finally a broad-spectrum immunoglobulin G antibody with high affinity with the original antigen is generated.

The invention provides an application of butyric acid in preparing a medicine for preventing and/or treating autoimmune diseases, and belongs to the technical field of autoimmune disease treatment. According to the embodiment of the invention, preventive intervention of butyric acid can obviously inhibit the occurrence and development of experimental arthritis, reduce the incidence rate of the arthritis by 74%, and protect articular synovial tissue from infiltration or erosion damage of inflammatory cells. The butyric acid can increase the expression of anti-inflammatory factor IL-10 while reducing the production of an autoantibody anti-CII and a pro-inflammatory factor IL-6. Furthermore, the butyric acid promotes the differentiation of joint lymph nodes and intestinal tract peyer's patches treg cells, and inhibits the expression of Tfh cells. The butyric acid can also down-regulate B cells of the germinal center of intestinal tract peyer's patches.

The invention discloses an application of substances capable of inhibiting activity of Treg cells and promoting differentiation of Tfh cells in treating HBV infection. The application provided by theinvention includes applications of a substance which is capable of inhibiting activity of regulatory T cells, a substance which is capable of scavenging the regulatory T cells and a reagent kit whichis composed of either the substance which is capable of inhibiting activity of the regulatory T cells or the substance which is capable of scavenging the regulatory T cells and an HBV vaccine as wellas applications of T follicular helper cells and germinal center B cells in preparing products for treating and/or preventing and/or diagnosing the HBV infection. Experiments prove that humoral immuneresponse disorder in a chronic HBV model mouse can be repaired by scavenging the Treg cells in vivo, and HBV scavenging can be promoted; by inhibiting functions of the Treg cells through intraperitoneal injection of a CTLA4 blocking antibody, so that the humoral immune response disorder in the chronic HBV model mouse can be repaired and HBV scavenging can be promoted. Therefore, by targeting to the regulatory T cells, functions of the regulatory T cells can be inhibited, the differentiation of HBV specific Tfh cells can be enhanced and HBV virus scavenging can be accelerated.

Provided are methods of determining cell of origin (COO) for diffuse large B Cell lymphoma (DLBCL) using DNA for the analysis. The methods include identification of DLBCL COO as activated B Cell (ABC) and germinal center B Cell (GCB).

The invention discloses a virus antigen-antibody compound vaccine for porcine epidemic diarrhea and a preparation method of the virus antigen-antibody compound vaccine, and belongs to the technical field of veterinary vaccines. The antigen-antibody compound vaccine is obtained by fully mixing a porcine epidemic diarrhea virus antigen and a porcine epidemic diarrhea virus antibody according to a volume ratio of 1: 5, penicillin with a final concentration of 1000 UI/mL and streptomycin with a final concentration of 1000 [mu]g/mL are added, and the vaccine is obtained by incubating at a temperature of 37 DEG C for 2 h. The antigen-antibody compound vaccine does not need to inactivate the antigen, so that live viruses in the antigen-antibody compound vaccine are effectively protected, and immune organs are induced to generate more immune germinal centers. The antibody in the compound vaccine plays a role in delaying virus release, and the Fc fragment of the antibody enables the compound tobe captured by antigen presenting cells more easily, so that immune response is caused. The virus antigen-antibody compound vaccine can break through a maternal antibody and induce a high-titer antibody, and has a good immune effect and a good challenge protection rate on suckling piglets, replacement pigs, sows and offspring piglets thereof.

The invention relates to applications of astemizole shown in formula (I) pharmaceutically acceptable salts or solvates thereof in preparing drugs for preventing and/or treating malignant lymphoma, an application of astemizole and pharmaceutically acceptable salts or solvates thereof as an inhibitor of polycomb repressive complex 2 (PRC2), and an application astemizole and pharmaceutically acceptable salts or solvates thereof as an inhibitor for EZH2-EED interaction. Malignant lymphoma is a disease related to B-cell lymphoma of the germinal center, and comprises hodgkin lymphoma and non-hodgkin lymphoma. In addition, astemizole, and the pharmaceutically acceptable salt or solvate thereof can be put in combination use with the EZH2 inhibitor. The formula (I) is shown in the description.

The invention provides for noninvasive assessment of immunocompetence in various situations, for example, when modified by disease or by immunomodulators. The assessment determines the functional activity of germinal centers via measuring levels of immunogolublin isotype class switching. The invention provides for assessment of therapeutic efficacy of immunomodulators and for selection of treatment regimens. The invention also provides for determining the risk or susceptibility to adverse events upon receipt of therapy. Compositions, kits and methods are described herein.

The present invention relates to compositions and methods of inhibiting stem cell binding to organs and tissues, including the blocking of stem cell binding to germinal centers present in lymph tissue. Disclosed are compositions and methods for regenerating germinal centers in lymphatic tissue. Included in the compositions are adjuvants, agonists to CD40, CD28 and the IL-21 receptor, and antagonist to CD20.

The present invention relates to glycosylate HIV timer nanoparticles fused to self-assembling ferritin proteins which may be utilized as immunogens to enhance trafficking to lymph nodes and germinal centers and to heighten immune responses.

The present invention provides a method for determining whether a Rheumatoid Arthritis (RA) patient is susceptible to treatment with a B cell targeted therapy, which method comprises the step of analysing B cells and/or germinal centre-like structures (GC-LS) in a synovial tissue sample from the patient; wherein a patient whose synovial tissue sample is B cell rich and/or GC-LS negative is determined to be susceptible to treatment with the B cell targeted therapy, whereas a patient whose synovial tissue sample is B-cell poor and/or GC-LS positive is determined to be resistant to treatment with the B cell targeted therapy.

Endophilin I is a brain-specific protein functioning in clathrin-mediated endocytosis. The present invention is based on the finding that the rat germinal center kinase-like kinase (rGLK), a member of the germinal center kinase (GCK) family of c-jun N-terminal kinase (JNK) activating enzymes, is a novel endophilin I-binding partner. In a first aspect of the present invention, the novel interaction between endophilin I and rGLK is put to use in a novel screening assay. In a second aspect of the present invention, the interaction between endophilin I and GLK is modulated for therapeutic purposes, namely for the prevention and/or curtailment of neurological disorders associated with the JNK pathway. JNK-mediated neuronal cell death is believed to play an important role in injuries and diseases involving neuronal degeneration, such as Huntington's disease.