Th17 Cells Pathways in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorders: Pathophysiological and Therapeutic Implications

• Published in: Mediators of inflammation Vol. 2016; no. 2016; pp. 1 - 11
• Main Authors: Fujihara, Kazuo, Becker, Jefferson, Sato, Douglas Kazutoshi, Passos, Giordani Rodrigues Dos
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2016; John Wiley & Sons, Inc; Hindawi Limited
• Subjects: Animals; Autoimmunity; Central Nervous System - drug effects; Central Nervous System - metabolism; Central Nervous System - pathology; Cytokines; Disease; Health aspects; Humans; Multiple sclerosis; Multiple Sclerosis - drug therapy; Multiple Sclerosis - metabolism; Multiple Sclerosis - pathology; Neurology; Neuromyelitis optica; Neuromyelitis Optica - drug therapy; Neuromyelitis Optica - metabolism; Neuromyelitis Optica - pathology; Pathogenesis; Pharmaceutical industry; Review; Rodents; Science; Studies; Th17 Cells - drug effects; Th17 Cells - metabolism
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1155/2016/5314541

Several animal and human studies have implicated CD4+ T helper 17 (Th17) cells and their downstream pathways in the pathogenesis of central nervous system (CNS) autoimmunity in multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD), challenging the traditional Th1-Th2 paradigm. Th17 cells can efficiently cross the blood-brain barrier using alternate ways from Th1 cells, promote its disruption, and induce the activation of other inflammatory cells in the CNS. A number of environmental factors modulate the activity of Th17 pathways, so changes in the diet, exposure to infections, and other environmental factors can potentially change the risk of development of autoimmunity. Currently, new drugs targeting specific points of the Th17 pathways are already being tested in clinical trials and provide basis for the development of biomarkers to monitor disease activity. Herein, we review the key findings supporting the relevance of the Th17 pathways in the pathogenesis of MS and NMOSD, as well as their potential role as therapeutic targets in the treatment of immune-mediated CNS disorders.