期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 45, 期 9, 页码 2628-2637出版社
WILEY-BLACKWELL
DOI: 10.1002/eji.201545553
关键词
CD4(+) T cell; CXCL8; IFN-gamma; IL-1; TCR; TLR
类别
资金
- Department of Biotechnology, Government of India through National Institute of Immunology
- Council of Scientific and Industrial Research, Govt. of India
Toll-like receptors (TLRs) play a major part in providing innate immunity against pathogenic microorganisms. Recent studies show that these receptors are also expressed on T cells, which are the sentinels of adaptive immunity. Here, we have investigated the regulatory role of the T-cell receptor in the functioning of these innate receptors in T cells. We show that freshly isolated human CD4(+) T cells readily secrete the neutrophil chemoattractant CXCL8 upon activation with the TLR ligands Pam3CSK and flagellin. In contrast, TCR-activated cells secrete considerably less CXCL8 but start producing IFN-gamma upon stimulation with TLR agonists in the absence of concomitant TCR engagement. These T cells show increased activation of p38 and JNK MAP-kinases in response to TLR stimulation, and inhibition of p38 abrogates TLR-induced IFN-gamma secretion. The shifting of the T-cell innate immune response from CXCL8(hi)IFN-gamma(null) in freshly isolated to CXCL8(lo)IFN-gamma(hi) in activated T cells is also observed in response to endogenous innate stimulus, IL-1. These results suggest that the innate immune response of human CD4(+) T cells switches from a proinflammatory to an effector type following activation of these cells through the antigen receptor.
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