Regulation of lymphocyte trafficking in central nervous system autoimmunity

• Published in: Current opinion in immunology Vol. 55; pp. 38 - 43
• Main Authors: Oukka, Mohamed, Bettelli, Estelle
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.12.2018
• ISSN: 0952-7915; 1879-0372
• DOI: 10.1016/j.coi.2018.09.008

•Sphingosine-1-phosphate (S1P) blocks the egress of naïve T cells, Th17, and TCM cells from the lymph nodes.•Inhibition of the S1P/S1P1 signaling alters the phenotype and function of Treg.•Treg can enter the CNS independently of VLA4.•In the absence of VLA4/VCAM-1 interaction, other adhesion molecules promote the entry of Treg and Th17 cells in the CNS. CD4+ T helper (Th) cells play a central role in orchestrating protective immunity but also in autoimmunity. Multiple Sclerosis (MS) is a human autoimmune disease of the central nervous system (CNS) characterized by the infiltration of inflammatory lymphocytes and myeloid cells into the brain and spinal cord, leading to demyelination, axonal damage, and progressive loss of motor functions. The release of T cells in the circulation and their migration in the central nervous system are key and tightly regulated processes which have been targeted to decrease CD4+ T cell presence in the CNS and limit disease progression. Here, we review two of these pathways and discuss how their blockade modulate different subsets of CD4+ T cells.