A Decade of Research on TLR2 Discovering Its Pivotal Role in Glial Activation and Neuroinflammation in Neurodegenerative Diseases.
- Author:
Jin Hee HAYWARD
1
;
Sung Joong LEE
Author Information
- Publication Type:Review
- Keywords: microglia; astrocytes; Schwann cells; neuropathic pain; stroke; intracerebral hemorrhage
- MeSH: Astrocytes; Brain Injuries; Cell Death; Cerebral Hemorrhage; Cerebral Hemorrhage, Traumatic; Humans; Immunity, Innate; Inflammation; Microglia; Nervous System; Nervous System Diseases; Neuralgia; Neurodegenerative Diseases*; Neuroglia; Neurons; Oligodendroglia; Receptors, Pattern Recognition; Schwann Cells; Stroke; Toll-Like Receptors
- From:Experimental Neurobiology 2014;23(2):138-147
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
