HMGB1-TLR Signaling in Rasmussens EncephalitisTianfu Li1,3,4,*, Qing Gao3 and Guoming Luan2,3,4
- *Corresponding Author:
- Tianfu Li
Professor and Chief Physician, Department of Neurology
Beijing Sanbo Brain Hospital, Capital Medical University
Xiangshan Yikesong 50, Haidian district
Beijing, 100093, P.R. China
Tel: +86 1062856761
E-mail: [email protected]
Received date: July 25, 2016; Accepted date: August 09, 2016; Published date: August 12, 2016
Citation: Li T, Gao Q, Luan G (2016) HMGB1-TLR Signaling in Rasmussens’ Encephalitis. J Neuroinfect Dis 7: 223. doi: 10.4172/2314-7326.1000223
Copyright: © 2016 Li T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Rasmussen’s encephalitis is neurological disorder of childhood characterized by uni-hemispheric inflammation, intractable focal epilepsy and progressive cognitive and neurological deficits. Currently, the pathogenesis of Rasmussen’s encephalitis is still enigmatic and hemispherectomy is the only effective method to control the seizures associated with Rasmussen’s encephalitis. Recently data indicated that intrinsic activation of endogenous proinflammation high-mobility group box-1 (HMGB1) and Toll-like receptor (TLR) is involved in the development of Rasmussen’s encephalitis. Activation of HMGB1-TLR signaling plays a critical role in brain inflammation, development of epilepsy and cognitive dysfunction. Targeted therapy on HMGB1-TLR signaling might be a novel strategy with anti-inflammation, anti-epilepsy as well as improving cognitive dysfunction associated with epilepsy in Rasmussen’s encephalitis.