Molecular Mimicry between Helicobacter pylori Antigens and H super(+),K super(+)-Adenosine Triphosphatase in Human Gastric Autoimmunity

Autoimmune gastritis and Helicobacter pylori-associated gastric atrophy develop through similar mechanisms involving the proton pump H super(+),K super(+)-adenosine triphosphatase as autoantigen. Here, we report that H. pylori-infected patients with gastric autoimmunity harbor in vivo-activated gast...

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Published inThe Journal of experimental medicine Vol. 198; no. 8; pp. 1147 - 1156
Main Authors Amedei, A, Bergman, M P, Appelmelk, B J, Azzurri, A, Benagiano, M, Tamburini, C, van der Zee, R, Telford, J L, Vandenbroucke-Grauls, CMJE, D'Elios, M M, Del Prete, G
Format Journal Article
LanguageEnglish
Published 20.10.2003
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Summary:Autoimmune gastritis and Helicobacter pylori-associated gastric atrophy develop through similar mechanisms involving the proton pump H super(+),K super(+)-adenosine triphosphatase as autoantigen. Here, we report that H. pylori-infected patients with gastric autoimmunity harbor in vivo-activated gastric CD4 super(+) T cells that recognize both H super(+),K super(+)-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.
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ISSN:0022-1007