Abstract
A critical component in triggering and progressing autoimmune multiple sclerosis (MS) is the deregulation of immune responses, including dysfunction of T regulatory cells (Tregs), critical participants in the pathogenetic context of inflammation. It has been found that miRNAs have a crucial role in the induction of MS because dysregulation of miRNAs can result in defects in immunological tolerance. In this investigation, we examined the miR-10a contribution to MS disorder by comparing the altered expression of miR-10a in peripheral blood mononuclear cells (PBMCs) of 40 MS patients to 40 healthy controls. Additionally, we examined Tregs’ frequency in MS patients in compare with healthy controls. We evaluated the secreted levels of anti-inflammatory cytokines, such as IL-10 and TGF-B, in the serum of MS patients and their expression level in healthy controls’ and patients’ peripheral blood mononuclear cells (PBMCs). Then, we assessed the correlation between miR-10a expression with Treg frequency and levels of anti-inflammatory cytokines in serum. PBMCs from MS patients had downregulated expression of miR-10a, and a substantial correlation was found between this expression and a reduction in Treg cells’ frequency and the secreted anti-inflammatory cytokines associated with Tregs’ diminished functionality. In summary, our research demonstrated a strong correlation between Tregs’ frequency, lower levels of cytokines linked to Treg function, and lower expression of miR-10a in PBMCs. So, the alteration of miR-10a can be utilized as a probable therapeutic target for the prevention and management of MS disorder. However, further examination is requisite before this strategy become practical for use in the clinical setting
Published Version
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