The glycolipid exoantigen derived from Chlamydia muridarum activates invariant natural killer T cells

作     者：Ying Peng Lei Zhao Sudhanshu Shekhar Lu Liu Hong Wang Qiang Chen Xiaoling Gao xi Yang Weiming Zhao 

作者机构：Department of Medical Microbiology Shandong University School of Medicine Jinan China Department of Medical Microbiology and Department of ImmunologyUniversity of Manitoba Winnipeg Manitoba Canada 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2012年第9卷第4期

页      面：361-366页

核心收录：

学科分类：0710[理学-生物学] 090601[农学-基础兽医学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 07[理学] 1001[医学-基础医学(可授医学、理学学位)] 071009[理学-细胞生物学] 09[农学] 0906[农学-兽医学] 

基　　金：supported by PhD Studentships for Oversea Study from Shandong University. a grant from Canadian Institutes of Health Research supported by grants from National Natural Sciences Foundation of China 

主　　题：CDld Chlamydia GLXA iNKT 

摘      要：The chlamydial glycolipid exoantigen （GLXA）, a glycolipid antigen derived from Chlamydia muridarum, has been implicated in chlamydial-host cell interaction. Although glycolipid antigens from Sphingomonas and related bacteria have been shown to activate invariant natural killer T （iNKT） cells, it is not yet known whether GLXA can activate these cells. In this study, we have for the first time investigated the role of GLXA in iNKT cell activation using in vitro as well as in vivo settings. First, we examined the effect of GLXA on iNKT cell activation in a cell-free antigen-presentation assay, and found that GLXA specifically stimulated iNKT1.4 hybridoma cell produce enhanced amounts of IL-2. Next, we analyzed the effect of pharmacological activation of iNKT cells by GLXA using iNKT cell-deficient （iNKT knockout （KO）） mice and bone marrow-derived dendritic cell （BMDC）-Iiver mononuclear cell （LMC） coculture system. On stimulation with GLXA, iNKT cells produced higher quantities of cytokines in a CD 1d-dependent fashion. More importantly, iNKT cells from GLXA-treated, but not from cell mock-treated, mice showed higher expression of activation marker, CD69, and enhanced production of interferon （IFN）-y and I L-4 in vivo. Cumulatively, these data provide evidence on the pharmacological ability of GLXA in specifically activating iNKT cells.