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Infection and Immunity, April 2003, p. 1755-1762, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.1755-1762.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Helicobacter pylori-Specific CD4+ CD25high Regulatory T Cells Suppress Memory T-Cell Responses to H. pylori in Infected Individuals

Anna Lundgren,1,2 Elisabeth Suri-Payer,3 Karin Enarsson,1,2 Ann-Mari Svennerholm,1,2 and B. Samuel Lundin1,2*

Department of Medical Microbiology and Immunology,1 Göteborg University Vaccine Research Institute (GUVAX),2 Department of Rheumatology and Inflammation Research, Göteborg University, 405 30 Göteborg, Sweden3

Received 12 August 2002/ Returned for modification 30 October 2002/ Accepted 18 December 2002

Helicobacter pylori colonizes the gastric and duodenal mucosa. The infection normally persists for life and causes peptic ulcers and gastric cancer in a subset of infected individuals. We hypothesized that the inability to clear the infection may be a consequence of H. pylori-specific regulatory T cells that actively suppress T-cell responses. Therefore, we characterized the T-cell responses to H. pylori in H. pylori-infected individuals without any subjective symptoms and in uninfected control subjects and investigated the role of regulatory CD4+ CD25high T cells during infection. The stimulation of CD4+ peripheral blood T cells with monocyte-derived dendritic cells pulsed with a membrane preparation of H. pylori resulted in proliferation and gamma interferon production in both infected and uninfected individuals. Sorted memory cells from infected individuals responded less than cells from uninfected subjects, and the unresponsiveness could be abolished by depletion of CD4+ CD25high regulatory T cells or the addition of interleukin 2. Furthermore, CD4+ CD25high T cells suppressed H. pylori-induced responses in cocultures with CD25low/- cells. Tetanus toxoid induced comparable responses in memory cells from infected and uninfected individuals in both the presence and the absence of regulatory T cells, suggesting that the suppression was H. pylori specific. In conclusion, we have shown that H. pylori-infected individuals have impaired memory CD4+ T-cell responses to H. pylori that are linked to the presence of H. pylori-specific regulatory T cells that actively suppress the responses.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, Göteborg University, Box 435, 40530 Göteborg, Sweden. Phone: 46-31-3424685. Fax: 46-31-826976. E-mail: samuel.lundin{at}microbio.gu.se.

Editor: A. D. O'Brien

Infection and Immunity, April 2003, p. 1755-1762, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.1755-1762.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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