Review Article

Exp Neurobiol 2014; 23(2): 138-147

Published online June 30, 2014

© The Korean Society for Brain and Neural Sciences

A Decade of Research on TLR2 Discovering Its Pivotal Role in Glial Activation and Neuroinflammation in Neurodegenerative Diseases

Jin Hee Hayward and Sung Joong Lee*

Department of Neuroscience and Physiology of School of Dentistry, and Interdisciplinary Program in Genetic Engineering, Seoul National University, Seoul 110-749, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-740-8649, FAX: 82-2-762-5107

Received: May 7, 2014; Revised: May 21, 2014; Accepted: May 23, 2014


Toll-like receptors (TLRs) belong to a class of pattern recognition receptors that play an important role in host defense against pathogens. TLRs on innate immune cells recognize a wide variety of pathogen-associated molecular patterns (PAMPs) and trigger innate immune responses. Later, it was revealed that the same receptors are also utilized to detect tissue damage to trigger inflammatory responses in the context of non-infectious inflammation. In the nervous system, different members of the TLR family are expressed on glial cells including astrocytes, microglia, oligodendrocytes, and Schwann cells, implicating their putative role in innate/inflammatory responses in the nervous system. In this regard, we have investigated the function of TLRs in neuroinflammation. We discovered that a specific member of the TLR family, namely TLR2, functions as a master sentry receptor to detect neuronal cell death and tissue damage in many different neurological conditions including nerve transection injury, intracerebral hemorrhage, traumatic brain injury, and hippocampal excitotoxicity. In this review, we have summarized our research for the last decade on the role of TLR2 in neuroinflammation in the above neurological disorders. Our data suggest that TLR2 can be an efficient target to regulate unwanted inflammatory response in these neurological conditions.

Keywords: microglia, astrocytes, Schwann cells, neuropathic pain, stroke, intracerebral hemorrhage