Mycobacterial signaling through toll-like receptors

被引:100
|
作者
Basu, Joyoti [1 ]
Shin, Dong-Min [2 ]
Jo, Eun-Kyeong [2 ]
机构
[1] Bose Inst, Dept Chem, Kolkata, India
[2] Chungnam Natl Univ, Sch Med, Dept Microbiol & Infect Signaling Network Res Ctr, Taejon 301747, South Korea
关键词
mycobacteria; vitamin D; autophagy; antimicrobial peptides; innate immunity; INNATE IMMUNE-RESPONSES; VITAMIN-D; TUBERCULOSIS; AUTOPHAGY; TLR2; ANTIBIOTICS; MATURATION; SURVIVAL; CELLS; BCG;
D O I
10.3389/fcimb.2012.00145
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Studies over the past decade have helped to decipher molecular networks dependent on Toll-like receptor (TLR) signaling, in mycobacteria-infected macrophages. Stimulation of TLRs by mycobacteria and their antigenic components rapidly induces intracellular signaling cascades involved in the activation of nuclear factor-KB and mitogen-activated protein kinase pathways, which play important roles in orchestrating proinflammatory responses and innate defense through generation of a variety of antimicrobial effector molecules. Recent studies have provided evidence that mycobacterial TLR-signaling cross talks with other intracellular antimicrobial innate pathways, the autophagy process and functional vitamin D receptor (VDR) signaling. In this article we describe recent advances in the recognition, responses, and regulation of mycobacterial signaling through TLRs,
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页数:6
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