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- Table of Contents
Information about Experimental Autoimmune Encephalomyelitis: 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.
Most recent studies have shown that Experimental Autoimmune Encephalomyelitis shares some biological mechanisms with arthritis, autoimmune-diseases, autoimmune-reaction, autoimmunity, cns-disorder, decreased-immunologic-activity-[pe], delayed-hypersensitivity, demyelinating-diseases, demyelination, diarrhea, encephalitis, encephalomyelitis, escherichia-coli-infections, inflammation, inflammatory-disorder, multiple-sclerosis, nervousness, neuritis, sclerosis, tissue-adhesions.
Among the many pathways, these few ones have gauged particular interests from scientists studying Experimental Autoimmune Encephalomyelitis, and have been seen in publications frequently: Cell Activation, Cell Adhesion, Cell Death, Cell Differentiation, Cell Proliferation, Cytokine Production, Hypersensitivity, Immune Response, Inflammatory Response, Localization, Myelination, Neuroprotection, Pathogenesis, Regeneration, Secretion, Sensitization, T Cell Activation, T Cell Proliferation, Tolerance Induction, Virulence
Quite a number of genes have been found to play important roles in Experimental Autoimmune Encephalomyelitis, such as CD4, CD80, CTLA4, HLA-E, IFNG, IL10, IL17A, IL2, IL4, IL6, MAG, MBL2, MBP, MOG, PDXP, PLP1, PRDX5, PRG2, PTHLH, 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.