Department of Chemistry, Bose Institute Kolkata, India.
Front Cell Infect Microbiol. 2012 Nov 23;2:145. doi: 10.3389/fcimb.2012.00145. eCollection 2012.
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-κB 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.
过去十年的研究有助于破译分枝杆菌感染的巨噬细胞中依赖 Toll 样受体 (TLR) 信号的分子网络。分枝杆菌及其抗原成分刺激 TLR 可迅速诱导参与核因子-κB 和丝裂原活化蛋白激酶途径激活的细胞内信号级联反应,这些途径在通过生成各种抗菌效应分子来协调促炎反应和先天防御方面发挥重要作用。最近的研究提供了证据表明,分枝杆菌 TLR 信号与其他细胞内抗菌先天途径、自噬过程和功能性维生素 D 受体 (VDR) 信号相互作用。本文描述了通过 TLR 识别、应答和调节分枝杆菌信号的最新进展。