expression of mir-326 in t cell-derived exosomes of patients with relapsing-remitting multiple sclerosis

Invasion of auto-reactive cd4+ t cells especially th17 into central nervous system (cns) is an underlying pathogenic mechanism in multiple sclerosis (ms). cd4+ t cells release exosomes which are enriched in micrornas, reflective of cell’s physiological or pathological condition. thus exosomes could be potent agents to provide quantitative and qualitative information about involved cells in ms. we investigated the expression of pathogenic micrornas in t cells-derived exosomes of ms patients or healthy controls. conventional t cells (tconv) derived from relapsing-remitting (rr) ms patients (n=10) and healthy controls (n=10) were purified and cultured for 3 days by soluble anti-cd3/cd28. exosomes were purified from cultured-t cells supernatants. the expression levels of exosomal mir-146a, mir-29a, mir-155, and mir-326 were quantified by real-time pcr. a statistically significant increased expression of mir-326 in tconv-derived exosomes was observed in rrms patients as compared with controls (7.5±1.88vs 2.51±0.9 p=0.03), on the contrary, no differences were found in the expression levels of mir-155, mir-146a, and mir-29a, in tconv-derived exosomes of patients as compared with controls (p>0.05). our results point to altered expression in exosome-derived micrornas. mir-326 was previously shown to play a role in the immunopathogenesis of ms by inducing th17 differentiation and maturation. therefore, mir-326 containing exosomes might also be a potential clinical target in course of ms. moreover, the deregulation of this mirna in exosomes may serve as a diagnostic and prognostic biomarker.