| Literature DB >> 21269729 |
Jin-Yu Zhang1, Tao Liu, Hong Guo, Xiao-Fei Liu, Yuan Zhuang, Shu Yu, Li Chen, Chao Wu, Zhuo Zhao, Bin Tang, Ping Luo, Xu-Hu Mao, Gang Guo, Yun Shi, Quan-Ming Zou.
Abstract
Th17 cells represent a novel subset of CD4(+) T cells, which is associated with Helicobacter pylori infection. In the present study, we investigated the potential role of Urease subunit B (UreB) in the induction of Th17 cell response. Co-cultured splenic lymphocytes from H. pylori-infected mice with the recombinant UreB (rUreB) elevated IL-17 secretion and caused an increase in the number of Th17 cells. The expression of IL-6 and IL-23 p19 was significantly increased in rUreB-stimulated macrophages. Whole cell protein (WCP) of UreB-deficient strain (UreB(-) strain) induced less Th17 cell responses than that of wild-type strain. In addition, subcutaneous and intranasal immunization of rUreB elicited antigen-specific Th17 cell responses. Intranasal immunization of rUreB reduced H. pylori colonization in the stomach, which was closely related with the increased rUreB-specific Th17 cell responses. These results suggest that UreB is an important protein which is able to elicit Th17 cell responses against H. pylori both in vivo and in vitro.Entities:
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Year: 2010 PMID: 21269729 DOI: 10.1016/j.imbio.2010.12.006
Source DB: PubMed Journal: Immunobiology ISSN: 0171-2985 Impact factor: 3.144