van Driel, Ian R., Baxter, Alan G. , Laurie, Karen L. , Zwar, Tricia D., La Gruta, Nicole L., Judd, Louise M., Scarff, Katrina L., Silveira, Pablo A., and Gleeson, Paul A. (2002) Immunopathogenesis, loss of T cell tolerance and genetics of autoimmune gastritis. Autoimmunity Reviews, 1 (5). pp. 290-297.

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Abstract

Over the past 10 years experimental autoimmune gastritis has been established as a highly defined model of organ-specific autoimmunity. Autoimmune gastritis represents one of the few autoimmune diseases in which the causative autoantigens, namely the gastric H/K ATPase α- and β-subunits, are defined. Furthermore, it has been clearly established that a CD4+ T cell response to the H/K ATPase β-subunit, in particular, is essential for the initiation of autoimmune gastritis. The immunopathology of autoimmune gastritis is due to a disruption of the normal developmental pathways of the mucosa, rather than a direct depletion of the end-stage parietal and zymogenic cells. CD4+CD25+ regulatory T cells were first described in experimental autoimmune gastritis and there has been a recent explosion of interest in the potential role of these immunoregulatory T cells in protection against a variety of autoimmune diseases. The availability of H/K ATPase deficient mice has begun to provide considerable insight into the basis for tolerance to the gastric autoantigens. Experimental autoimmune gastritis has also provided valuable insight into our understanding of the genetics of disease susceptibility and four distinct genetic regions have been identified which confer susceptibility to this organ-specific disease. The highlights of these recent advances are the subject of this review.

Item ID:	12088
Item Type:	Article (Research - C1)
ISSN:	1568-9972
Date Deposited:	19 Oct 2010 00:58
FoR Codes:	11 MEDICAL AND HEALTH SCIENCES > 1107 Immunology > 110703 Autoimmunity @ 100%
SEO Codes:	97 EXPANDING KNOWLEDGE > 970111 Expanding Knowledge in the Medical and Health Sciences @ 100%
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