Review
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World J Biol Chem. Jul 26, 2011; 2(7): 167-172
Published online Jul 26, 2011. doi: 10.4331/wjbc.v2.i7.167
Toll-like receptors are potential therapeutic targets in rheumatoid arthritis
Siamak Sandoghchian Shotorbani, Zhao-Liang Su, Hua-Xi Xu
Siamak Sandoghchian Shotorbani, Zhao-Liang Su, Hua-Xi Xu, Department of Immunology, Institute of Laboratory Medicine, Jiangsu University, Zhenjiang 212013, Jiangsu Province, China
Author contributions: Shotorbani SS drafted the manuscript; Su ZL and Xu HX revised it; Xu HX also was the supervisor.
Supported by The National Natural Science Foundation of China (30871193, 30972748, 81001319), the Natural Science Foundation of Colleges and Universities in Jiangsu Province and Innovation Fund for Candidate of Doctor in Jiangsu Province (Grant No. 09KJB310001 and CX09B_217Z, respectively)
Correspondence to: Hua-Xi Xu, PhD, Professor, Department of Immunology, Institute of Laboratory Medicine, Jiangsu University, 301 Xuefu Road, Zhenjiang 212013, Jiangsu Province, China. xuhx@ujs.edu.cn
Telephone: +86-511-85038140 Fax: +86-511-85038449
Received: May 2, 2011
Revised: July 14, 2011
Accepted: July 21, 2011
Published online: July 26, 2011
Abstract

Toll-like receptors (TLRs) are found on the membranes of pattern recognition receptors and not only play important roles in activating immune responses but are also involved in the pathogenesis of inflammatory disease, injury and cancer. Furthermore, TLRs are also able to recognize endogenous alarmins released by damaged tissue and necrosis and/or apoptotic cells and are present in numerous autoimmune diseases. Therefore, the release of endogenous TLR ligands plays an important role in initiating and driving inflammatory diseases. Increasing data suggest a role for TLR signaling in rheumatoid arthritis, which is an autoimmune disease. Although their involvement is not comprehensively understood, the TLRs signaling transducers may provide potential therapeutic targets.

Keywords: Autoimmune disease, Innate immunity, Pattern recognition receptors, Rheumatoid arthritis, Toll-like receptors