ISSN: 2161-1149 (Printed)
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.