BM-MSCs ameliorate experimental autoimmune encephalomyelitis via modifying the expression of miR-193, miR-146a, miR-155, miR-21 and miR-326

Abstract Background: Experimental Autoimmune Encephalomyelitis (EAE) is a demyelinating neurological illness having immunological, histological, and clinical parallels to MS (EAE). Cell-to-cell communication and exosomes are two mechanisms through which MSCs exert their effects. The purpose of this study was to see how effective BM-MSCs were at treating EAE patients.Materials and Procedures: Myelin Oligodendrocyte Glycoprotein (MOG35-55) was used to induce EAE in C57BL/6 mice (n=32), and then BM-MSCs 1×106 cells were administered. Every day, clinical and weight examinations were performed. Histology will be used to assess inflammation and demyelination in mouse CNS parts. Using Real-time PCR, we investigated the expression of pro and anti-inflammatory genes, as well as miRNAs intricate in the differentiation and function of Th cells in the control and progression of EAE.Results: In the EAE, BM.MSCs significantly reduced clinical symptoms, inflammation, and demyelination of the brain. Our findings suggest that improved expression of miR-193 miR-146a and decreased expression of miR-155 and miR-21 miR-326 was followed by an increase in cytokine expression levels of IL-10, TGF-β, and IL-4; however, IFN-γ and IL-27 levels were reduced in treatment groups. Treatment groups were also associated with suppressing effects on Th1 and Th17 immune responses, induction of Treg cells, and immunoregulatory responses.Conclusions: These findings provide compelling evidence that MSC-derived exosomes modulate immune suppression and highlight the significance of BM.MSCs and miRNAs in affecting T cell differentiation and reducing CNS inflammation, demyelination, and local neurodegeneration.