Navigating through the maze of TLR2 mediated signaling network for better mycobacterium infection control.

Abstract

Toll-like receptor 2 (TLR2), a member of pattern recognition receptors (PRRs) abundant on macrophages, dendritic cells (DCs) and respiratory epithelial cells lining the lung, plays critical role in host immune response against Mycobacterium tuberculosis (MTB) infection. TLR2-mediated elimination of MTB involves multiple pathways such as promoting DCs maturation, generating biased Th1, Th2, Th17 type response, regulating the macrophage activation and cytokine secretion. MTB can also hijack the TLR2 signaling to subvert the host immunity by dampening the macrophages response to IFN-γ, suppressing the processing and presentation of antigens. This review summarizes the intricate network of TLR2-mediated signaling and Mycobacteria effectors involved in MTB-host interaction with an aim to find better target for improved tuberculosis control, especially the host-derived therapy targets. TLR2 agonists with potential to be included in novel tuberculosis vaccines are also discussed.

• Authors: Xiaowen Yu, Jie Zeng, Jianping Xie
• Journal: Biochimie (Biochimie) Vol. 102 Pg. 1-8 (Jul 2014) ISSN: 1638-6183 [Electronic] France
• PMID: 24594065 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2014 Elsevier Masson SAS. All rights reserved.

Chemical References

• TLR2 protein, human
• Toll-Like Receptor 2

Topics

• Dendritic Cells (immunology, microbiology)
• Host-Pathogen Interactions (genetics)
• Humans
• Immunity, Innate (genetics)
• Macrophages (immunology, microbiology)
• Mycobacterium tuberculosis (genetics, pathogenicity)
• Signal Transduction (genetics)
• Toll-Like Receptor 2 (genetics, immunology, metabolism)
• Tuberculosis (genetics, immunology, microbiology)