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Infection and Immunity, March 2008, p. 1289-1297, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.00779-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

CD8⁺ T Cells Are Associated with Severe Gastritis in Helicobacter pylori- Infected Mice in the Absence of CD4⁺ T Cells

Department of Microbiology and Immunology and The Australian Bacterial Pathogenesis Program, University of Melbourne, Melbourne, Victoria 3010, Australia,¹ Cooperative Research Centre for Vaccine Technology, Department of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria 3010, Australia,² Tissupath Pty. Ltd., Melbourne, Victoria 3122, Australia,³ The Walter and Eliza Hall Institute, Melbourne, Victoria 3050, Australia,⁴ CSL Limited, Melbourne, Victoria 3052, Australia⁵

Received 8 June 2007/ Returned for modification 16 July 2007/ Accepted 1 November 2007

Helicobacter pylori infection results in the development of chronic gastritis, and CD4⁺ T cells are a major component of the gastric cellular infiltrate. To examine whether CD4⁺ T cells are important in initiating and maintaining H. pylori-induced gastritis, mice deficient in CD4⁺ T cells (B6.BM1.GK 1.5 mice [GK 1.5 mice]) were infected with H. pylori. We found that as in normal mice, H. pylori-specific antibodies, mostly of the immunoglobulin M isotype, developed in GK 1.5 mice but were unable to cure H. pylori infection. Further, while the stomachs of H. pylori-infected GK 1.5 mice were more heavily infiltrated with CD8⁺ T cells and B cells, mice deficient in both CD4⁺ and CD8⁺ T cells developed mild inflammation comparable to the level observed for C57BL/6 mice. These observations suggest that CD4⁺ T cells may play an important role in regulating or suppressing gastric CD8⁺ T cells which, in the absence of CD4⁺ T cells, may mediate more-severe disease. These studies have revealed a potentially important role for CD8⁺ T cells in the gastric disease resulting from H. pylori infection.

Published ahead of print on 19 November 2007.

Editor: R. P. Morrison