This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
, No Gclids
Disease Info Card
Hypergammaglobulinemia
Information about Hypergammaglobulinemia: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Hypergammaglobulinemia
Most recent studies have shown that Hypergammaglobulinemia shares some biological mechanisms with acquired-immunodeficiency-syndrome, anemia, autoimmune-diseases, autoimmune-reaction, eosinophilia, hepatitis, hiv-infections, immunologic-deficiency-syndromes, infective-disorder, jobs-syndrome, lupus-erythematosus-systemic, lymphoma, malignant-paraganglionic-neoplasm, monoclonal-gammapathies, monoclonal-gammopathy-of-undetermined-significance, multiple-myeloma, neoplasms, polyclonal-hypergammaglobulinemia, sjogrens-syndrome.
Among the many pathways, these few ones have gauged particular interests from scientists studying Hypergammaglobulinemia, and have been seen in publications frequently: B Cell Activation, B Cell Differentiation, Cell Activation, Cell Death, Cell Differentiation, Cell Proliferation, Chemotaxis, Coagulation, Cytokine Production, Excretion, Hypersensitivity, Immune Response, Immunoglobulin Production, Isotype Switching, Localization, Lymphocyte Activation, Neutrophil Chemotaxis, Pathogenesis, Phagocytosis, Secretion
Quite a number of genes have been found to play important roles in Hypergammaglobulinemia, such as ALB, C3, CD4, CD40, CD40LG, CD8A, CRP, CTLA4, FAS, HLA-DQA1, IFNG, IL10, IL2, IL4, IL6, MVK, NOD2, SSB, TNF. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.