Abstract:
: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.
journal_name
Curr Top Microbiol Immunoljournal_title
Current topics in microbiology and immunologyauthors
McHugh RSdoi
10.1007/3-540-27702-1_8subject
Has Abstractpub_date
2005-01-01 00:00:00pages
153-77eissn
0070-217Xissn
2196-9965journal_volume
293pub_type
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