Immunopathogenesis, loss of T cell tolerance and genetics of autoimmune gastritis.

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