Affiliations: [a] Universidad Autónoma del Estado de Hidalgo (UAEH), Escuela Superior de Apan (ESAp), Laboratorio de Ingeniería en Biociencias, Carretera Apan-Calpulalpan Km. 8, Col. Chimalpa, Apan, Hidalgo, México | [b] Universidad Nacional Autónoma de México (UNAM), Facultad de Estudios Superiores Iztacala (FES-I), Unidad de Biomedicina (UBIMED), Laboratorio de Inmunoparasitología (Lab. 8), Av. de los Barrios #1, Los Reyes Iztacala, Tlalnepantla, Estado de México, México
Correspondence to: Luis I. Terrazas, Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, UNAM, México. Tel.: +52 56231333/ Ext. 39794; E-mail: email@example.com.
Abstract: Multiple sclerosis (MS) is an autoimmune disease that affects the central nervous system (CNS), mainly in dependency upon a complex interplay between lymphocytes and innate cells. As such, the role for hematopoietic cells, their extravasation into the CNS and their mechanisms for neurodegeneration have been extensively studied and discussed elsewhere. On the other hand, neurons, oligodendrocytes, astrocytes and microglia also produce mediators that contribute to the local microenvironment and either regulate or potentiate neurodegeneration, but their contribution to the whole phenomenon has been largely neglected. In this review we will address the crosstalk between neurons, glial cells and the immune system, discussing the neuroimmune interactions that may serve as important targets for future drug development.