upregulation of cd4+ t-cell derived mir-223 in the relapsing phase of multiple sclerosis patients

objective: micrornas (mirna) are a class of non-coding rnas which play key roles in post-transcriptional gene regulation. previous studies indicate that mirnas are dysregulated in patients with multiple sclerosis (ms). th17 and regulatory t (treg) cells are two subsets of cd4+ t-cells which have critical functions in the onset and progression of ms. the current study seeks to distinguish fluctuations in expression of cd4+ t-cell derived mir-223 during the relapsing-remitting (rr) phase of ms (rr-ms), as well as the expressions of th17 and treg cell markers. materials and methods: this experimental study used real-time quantitative polymerase chain reaction (qrt-pcr) to evaluate cd4+ t cell derived mir-223 expression patterns in patients that experienced either of the rr-ms phases (n=40) compared to healthy controls (n=12), along with rna markers for th17 and treg cells. we conducted flow cytometry analyses of forkhead box p3 (foxp3) and rar-related orphan receptor γt (rorγt) in cd4+ t-cells. putative and validated targets of mir-223 were investigated in the mirwalk and mirtarbase databases, respectively. results: mir-223 significantly upregulated in cd4+ t-cells during the relapsing phase of rr-ms compared to the remitting phase (p=0.000) and healthy individuals (p=0.036). expression of rorγt, a master transcription factor of th17, upregulated in the relapsing phase, whereas foxp3 upregulated in the remitting phase. additionally, potential targets of mir-223, stat1, forkhead box o (foxo1) and foxo3 were predicted by in silico studies. conclusion: mir-223 may have a potential role in ms progression. therefore, suppression of mir-223 can be proposed as an appropriate approach to control progression of the relapsing phase of ms.