Abstract
Host specific T-cell response is critical for the outcome of Helicobacter pylori infection. In genetically susceptible individuals, H. pylori can activate gastric CD4+ Th1 cells that recognize cross-reactive epitopes shared by H. pylori proteins and self H+, K+-ATPase, leading to gastric autoimmunity via molecular mimicry.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antigens, Bacterial / immunology
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Autoantigens / immunology
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Autoimmunity*
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Gastritis / enzymology
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Gastritis / immunology
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Gastritis / microbiology*
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Helicobacter Infections / immunology
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Helicobacter pylori / immunology*
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Humans
Substances
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Antigens, Bacterial
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Autoantigens