The Balance of Th17 Versus Treg Cells in Multiple Sclerosis

Among the wide range of the central nervous system (CNS)-related diseases multiple sclerosis (MS) has drawn much attention these days. MS is considered as a chronic autoinflammatory disorder, which leads to brain inflammation and may involve a break tolerance.Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS. MS is characterized based on Antigen-reactive T cells with distinct cytokine secretion resulting in attacking myelin sheaths around axons in the brain and spinal cord. Although previously itwas considered that Th1 cell subset drives MS, today it is demonstrated that pathogenic Th17 cells and the impaired balance of Th17/Treg axis are implicated in the pathogenesis of MS. Th17 key cytokines play an important role in MS. As an example, IL-17, the hallmarkcytokine of Th17, induces neutrophils infiltrations and ILs productions. It also shows a positive correlation with MS severity. IL-6 and tumor growth factor β (TGF-β), two main cytokines in Th17 differentiation affect neurogenesis like glial cells. IL-1 β is also involved in this process via disrupting blood-brain barrier, enhancing microglia and astrocytes activity resulting in accelerating nerve cell demyelination. Regulatory Tcells (Treg) are also implicated in the pathogenesis of MS. They can decrease MS progression, and depletion of Tregs exacerbates EAE. Also, IL-10, secreted by Tregs attenuates EAE severity. Overall, Th17 and Treg special cytokines and factors leading to an imbalance ofTh17/Treg axis are considered to be essential in MS and EAE immunopathogenesis. In this review, we covered various factors, which can cause an imbalance between Th17 and Treg subsets in MS and EAE