Molecular mimicry between Helicobacter pylori antigens and H+, K+ --adenosine triphosphatase in human gastric autoimmunity.

A Amedei, M.P. Bergman, B.J. Appelmelk, A Azzurri, M Benagiano, C Tamburini, R van der Zee, JL Telford, C.M.J.E. Vandenbroucke-Grauls, MM D'Elios, G Del Prete

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Abstract

Autoimmune gastritis and Helicobacter pylori-associated gastric atrophy develop through similar mechanisms involving the proton pump H+,K+-adenosine triphosphatase as autoantigen. Here, we report that H. pylori-infected patients with gastric autoimmunity harbor in vivo-activated gastric CD4+ T cells that recognize both H+, K+-adenosine triphosphatase and H. pylori antigens. We characterized the submolecular specificity of such gastric T cells and identified cross-reactive epitopes from nine H. pylori proteins. Cross-reactive H. pylori peptides induced T cell proliferation and expression of T helper type 1 functions. We suggest that in genetically susceptible individuals, H. pylori infection can activate cross-reactive gastric T cells leading to gastric autoimmunity via molecular mimicry.
Original languageEnglish
Pages (from-to)1147-56
JournalJournal of Experimental Medicine
Volume198
Issue number8
DOIs
Publication statusPublished - 2003
Externally publishedYes

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