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Infect. Immun. doi:10.1128/IAI.01063-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Resistance of primary murine CD4⁺ T cells to Helicobacter pylori vacuolating cytotoxin (VacA)

Department of Medicine and Microbiology and Immunology, Vanderbilt University School of Medicine, and Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee

^* To whom correspondence should be addressed. Email: timothy.L.cover{at}vanderbilt.edu.

	Abstract

Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for development of gastric cancer and peptic ulcer disease. H. pylori secretes a toxin, VacA, that targets human gastric epithelial cells and T lymphocytes and enhances the ability of H. pylori to colonize the stomach in a mouse model. To examine how VacA contributes to H. pylori colonization of the mouse stomach, we investigated whether murine T lymphocytes were susceptible to VacA activity. VacA inhibited IL-2 production by a murine T cell line (LBRM-33), similar to its effects on a human T cell line (Jurkat), but did not inhibit IL-2 production by primary murine splenocytes or CD4⁺ T cells. VacA inhibited activation-induced proliferation of primary human CD4⁺ T cells, but did not inhibit proliferation of primary murine CD4⁺ T cells. Flow cytometry studies indicated that the levels of VacA binding to primary murine CD4⁺ T cells were significantly lower than levels of VacA binding to human CD4⁺ T cells. This suggests that the resistance of primary murine CD4⁺ T cells to VacA is attributable, at least in part, to impaired VacA binding to these cells.

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