| Literature DB >> 18025102 |
Mai Ping Tan1, John Pedersen, Yifan Zhan, Andrew M Lew, Martin J Pearse, Odilia L C Wijburg, Richard A Strugnell.
Abstract
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.Entities:
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Year: 2007 PMID: 18025102 PMCID: PMC2258850 DOI: 10.1128/IAI.00779-07
Source DB: PubMed Journal: Infect Immun ISSN: 0019-9567 Impact factor: 3.441