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Resistance of Primary Murine CD4⁺ T Cells to Helicobacter pylori Vacuolating Cytotoxin

Holly M. Scott Algood,¹ Victor J. Torres,² Derya Unutmaz,^2, and Timothy L. Cover^1,2,3*

Departments of Medicine,¹ Microbiology and Immunology, Vanderbilt University School of Medicine,² Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee³

Received 6 July 2006/ Returned for modification 14 August 2006/ Accepted 16 October 2006

Persistent colonization of the human stomach by Helicobacter pylori is a risk factor for the 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 interleukin-2 (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 the 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.

Published ahead of print on 30 October 2006.

Editor: D. L. Burns

Present address: New York University School of Medicine, Joan and Joel Smilow Research Center, 522 First Avenue, Smilow 10th Floor, Rm. 1011, New York, NY 10016.

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