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Protection against H. pylori is IL-12-dependent and mediated by Th1 cells.

Vaccine Weekly

| February 12, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 FEB 12 - (NewsRx.com & NewsRx.net) -- "The regulatory roles of Th1 and Th2 cells in immune protection against Helicobacter infection are not clearly understood. In this study, we report that a primary H. pylori infection can be established in the absence of IL-12 or IFN-gamma," researchers in Sweden and the United States report.

"However, IFN-gamma, but not IL-12, was involved in the development of gastritis because IFN-gamma(-/-) (GKO) mice exhibited significantly less inflammation as compared with IL-12(-/-) or wild-type (WT) mice," said Ali A. Akhiani and colleagues at the University of Goteborg in Sweden and AstraZeneca R&D Boston in the United States. "Both IL-12(-/-) and GKO mice failed to develop protection following oral immunization with H. pylori lysate and cholera toxin adjuvant. By contrast, Th2-deficient, IL-4(-/-), and WT mice were equally well protected."

The investigators found that "mucosal immunization in the presence of co-administered rIL-12 in WT mice increased antigen-specific IFN-gamma-producing T cells by 5-fold and gave an additional 4-fold reduction in colonizing bacteria, confirming a key role of Th1 cells in protection. Importantly, only protected IL-4(-/-) and WT mice demonstrated substantial influx of CD4+ T cells in the gastric mucosa. The extent of inflammation in challenged IL-12(-/-) and GKO mice was much reduced compared with that in WT mice, indicating that IFN-gamma/Th1 cells also play a major role in postimmunization gastritis. Of note, ...

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Source: HighBeam Research, Protection against H. pylori is IL-12-dependent and mediated by Th1...

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