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.
Molecular mimicry between Helicobacter pylori antigens and H/K-ATPase in human gastric autoimmunity / A. AMEDEI; BERGMAN M.P.; APPELMELK B.J.; AZZURRI A.; BENAGIANO M.; TAMBURINI C.; VAN DER ZEE R.; TELFORD J.L.; VANDENBROUCKE-GRAULS C.M.; D'ELIOS M.M.; DEL PRETE G.. - In: JOURNAL OF EXPERIMENTAL MEDICINE. - ISSN 0022-1007. - STAMPA. - 198:(2003), pp. 1147-1156. [10.1084/jem.20030530]
Molecular mimicry between Helicobacter pylori antigens and H/K-ATPase in human gastric autoimmunity.
AMEDEI, AMEDEO;D'ELIOS, MARIO MILCO;DEL PRETE, GIANFRANCO
2003
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.File | Dimensione | Formato | |
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JEM 2003 corresponding author D'Elios.pdf
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