Nuclear Receptor Control of Myeloid Cell Responses - Implications for CNS Autoimmunity
- *Corresponding Author:
- Luisa Klotz
Department für Neurologie, Klinik für Allgemeine Neurologie
Universitätsklinikum Münster, Germany
E-mail: [email protected]
Received date: July 29, 2013; Accepted date: September 30, 2013; Published date: October 07, 2013
Citation: Hucke S, Wiendl H, Knolle P, Klotz L (2013) Nuclear Receptor Control of Myeloid Cell Responses - Implications for CNS Autoimmunity. Rheumatology 3:124. doi: 10.4172/2161-1149.1000124
Copyright: © 2013 Hucke S, 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.
During autoimmunity of the central nervous system (CNS), such as Multiple Sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE), myeloid cells play a central role in shaping the local inflammatory milieu and significantly contribute to the extent of disease pathology. Myeloid cells contribute to local reactivation of encephalitogenic T cells and, through production of pro-inflammatory mediators, also promote neurotoxicity and demyelination. In contrast, myeloid cells that acquired an anti-inflammatory phenotype ameliorate CNS autoimmunity and significantly contribute to resolution of inflammation. In this review we will discuss the role of selected nuclear receptors in modifying myeloid cell immune responses during autoimmune inflammation of the CNS and their potential as new targets for treatment regimens in MS.