Significant Role(s) of CXCL12 and the SDF-1 3'A Genetic Variant in the Pathogenesis of Multiple Sclerosis.

Both cellular and molecular components of the immune system are among the substantial factors involved in the pathogenesis of multiple sclerosis (MS). Accumulating evidence confirms that chemokines, as the main members of the immune system, play key roles in the regulation of immune responses. Immune system genetic parameters are believed to influence the onset of immune system-related diseases. Regarding the significant role of the CXCR4/CXCL12 axis in cell differentiation and survival and homing of hematopoietic progenitors to the bone marrow and regulation of neuronal progenitor cell migration in the central nervous system (CNS), genetic factors can cause an increased expression of CXCL12 and induce a vigorous immune response against CNS antigens in MS patients. Previous studies have indicated that the expression of CXCL12 could be affected by its polymorphisms at position +801 at the region of the CXCL12 3'A genetic variation. Finally, CXCL12 seems to be involved in the cellular part of the events that take place in the CNS, and therefore it could be considered as a target in MS therapies. Thus, this review was aimed to describe the recent progress in understanding the role of CXCL12 in MS, with an emphasis on CXCL12 serum concentrations and its gene polymorphism at position +801.