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International Reviews of Immunology Volume 24, 2005 - Issue 1-2
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The Story So Far: Helicobacter Pylori and Gastric Autoimmunity

Mathijs P. Bergman Department of Medical Microbiology and Infection Control, VU Medical Center, Amsterdam, The Netherlands
,
Christina M. J. E. Vandenbroucke-Grauls Department of Medical Microbiology and Infection Control, VU Medical Center, Amsterdam, The Netherlands
,
Ben J. Appelmelk Department of Medical Microbiology and Infection Control, VU Medical Center, Amsterdam, The Netherlands
,
Mario M. D'Elios Department of Internal Medicine and Immunoallergology, University of Florence, Florence, Italy
,
Amedeo Amedei Department of Internal Medicine and Immunoallergology, University of Florence, Florence, Italy
,
Annalisa Azzurri Department of Internal Medicine and Immunoallergology, University of Florence, Florence, Italy
,
Marisa Benagiano Department of Internal Medicine and Immunoallergology, University of Florence, Florence, Italy
&
Gianfranco Del Prete Department of Internal Medicine and Immunoallergology, University of Florence, Florence, Italy
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Pages 63-91 | Published online: 03 Aug 2009
 
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Abstract

The gastric mucosal pathogen Helicobacter pylori induces autoantibodies directed against the gastric proton pump H+,K+-ATPase in 20–30% of infected patients. The presence of these autoantibodies is associated with severity of gastritis, increased atrophy, and apoptosis in the corpus mucosa, and patients with these autoantibodies infected with H. pylori display histopathological and clinical features that are similar to those of autoimmune gastritis (AIG). This review will focus on the T helper cell responses, cytokines, and adhesion molecules involved in corpus mucosal atrophy in chronic H. pylori gastritis and in AIG, and the role of H. pylori in the onset of AIG.

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