The essential roles of Toll-like receptor signaling pathways in sterile inflammatory diseases

Qing Lin; Mingcai Li; Dan Fang; Jiazhu Fang; Shao Bo Su

doi:10.1016/j.intimp.2011.04.026

The essential roles of Toll-like receptor signaling pathways in sterile inflammatory diseases

Qing Lin, Mingcai Li, Dan Fang, Jiazhu Fang, Shao Bo Su

Research output: Contribution to journal › Review article › peer-review

Abstract

Toll-like receptors (TLRs) form a family of pattern recognition receptors with at least 11 members in human and 13 in mouse. TLRs recognize a wide variety of putative host-derived agonists that have emerged as key mediators of innate immunity. TLR signaling also plays an important role in the activation of the adaptive immune system by inducing pro-inflammatory cytokines and upregulating costimulatory molecules of antigen presenting cells. Inappropriate activation of TLRs by self-components generated by damaged tissues may result in sterile inflammation. This review discusses the contribution of TLR signaling to the initiation and progression of non-infectious inflammatory processes, such as ischemia and reperfusion (I/R) injury, tissue repair and regeneration and autoimmune diseases. The involvement of TLR signaling in the pathogenesis of sterile inflammation-related diseases may provide novel targets for the development of therapeutics.

Original language	English (US)
Pages (from-to)	1422-1432
Number of pages	11
Journal	International Immunopharmacology
Volume	11
Issue number	10
DOIs	https://doi.org/10.1016/j.intimp.2011.04.026
State	Published - Oct 1 2011
Externally published	Yes

Keywords

Autoimmunity
Ligands
Sterile inflammation
Toll-like receptors

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Pharmacology

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abstract = "Toll-like receptors (TLRs) form a family of pattern recognition receptors with at least 11 members in human and 13 in mouse. TLRs recognize a wide variety of putative host-derived agonists that have emerged as key mediators of innate immunity. TLR signaling also plays an important role in the activation of the adaptive immune system by inducing pro-inflammatory cytokines and upregulating costimulatory molecules of antigen presenting cells. Inappropriate activation of TLRs by self-components generated by damaged tissues may result in sterile inflammation. This review discusses the contribution of TLR signaling to the initiation and progression of non-infectious inflammatory processes, such as ischemia and reperfusion (I/R) injury, tissue repair and regeneration and autoimmune diseases. The involvement of TLR signaling in the pathogenesis of sterile inflammation-related diseases may provide novel targets for the development of therapeutics.",

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