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Interferon-gamma secretion is induced in IL-12 stimulated human NK cells by recognition of Helicobacter pylori or TLR2 ligands

Journal article
Authors Åsa Lindgren
Voja Pavlovic
Carl-Fredrik Flach
Åsa Sjöling
Samuel B Lundin
Published in Innate Immunity
Volume 17
Issue 2
Pages 191-203
ISSN 1753-4267
Publication year 2011
Published at Institute of Biomedicine, Department of Microbiology and Immunology
Pages 191-203
Language en
Links dx.doi.org/10.1177/1753425909357970
Subject categories Microbiology in the medical area

Abstract

Helicobacter pylori induce a chronic inflammation in the human gastric mucosa characterized by increased production of interferon-gamma (IFN-γ). The presence of natural killer (NK) cells in the human gastric mucosa and the ability of NK cells to produce IFN-γ suggest an important role of NK cells in the immune response directed towards H. pylori infection. Since NK cells previously have been shown to respond to bacterial components with IFN-γ production, we investigated the mechanisms for the recognition of H. pylori. We found that inhibition of MyD88 homodimerization resulted in decreased production of IFN-γ and that inhibition of the p38 MAPK decreased the production as well as the secretion of IFN-γ. Further studies indicated an involvement of Toll-like receptors (TLRs), in particular TLR2. Finally, we showed that the H. pylori specific membrane bound lipoprotein HpaA induced IFN-γ production from NK cells through recognition by TLR2. In conclusion, we suggest an involvement of TLR2 in the recognition of H. pylori by human NK cells and that HpaA is a TLR2 ligand important for recognition.

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