Autoimmune gastritis is a well-defined autoimmune disease model for the study of CD4+CD25+ T cell-mediated suppression.
Autoimmune gastritis (AIG) is an experimental model that closely resembles human autoimmune gastritis, the underlying pathology of pernicious anemia. Pathogenic CD4+ T cells are reactive to the parietal cell autoantigen, H/K ATPase, and are controlled by CD4+CD25+ T cells in an immunosuppressive cytokine-independent manner. Comparison of CD4+CD25+ T cell-mediated suppression in other autoimmune models shows inconsistencies with respect to requirements of cytokines for immunosuppression. More recent data, however, indicate that the evidence for requirement of IL-10 and TGF-beta could be due to the complex nature of the T cells causing the disease as well as the role of induced regulatory T cell populations. AIG provides a well-defined model that may allow for better analysis of CD4+CD25+ T cell in vivo biology. Evidence from this model indicates that immune responses must be initiated and then CD4+CD25+ T cells are recruited to control the quality of the immune response.
Malaghan Institute of Medical Research, 6001 Wellington, New Zealand. rmchugh@malaghan.org.nz
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D000752:Anemia, Pernicious / Q000276:immunology; D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D005756:Gastritis / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance; D015375:Receptors, Interleukin-2 / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D015375:Receptors, Interleukin-2