Objective: MiR-181a plays a critical role in modulating T cell and B cell differentiation, as well as immune response. Its abnormal expression probably participates in the pathogenesis of systemic lupus erythematosus (SLE). MiR-203 is involved in regulating Toll-like receptor and inducing immune tolerance. Abnormal expression or function of miR-203 is related to multiple auto-immune diseases but its role in SLE remains unclear. This study, thus, investigated the serum level of miR-181a and miR-203, to analyze their roles in diagnosing and evaluating SLE.
Patients and methods: SLE patients were recruited from our hospital, and divided into non-active and active SLE based on disease activity index, along with healthy individuals. qRT-PCR was used to quantify the serum miR-181a and miR-203 expression, and their correlation with clinical features. ROC was used to evaluate the diagnostic value on SLE, while survival curves were compared to show progression-free survival (PFS) between populations with high and low expression.
Results: SLE patients had significantly higher serum levels of miR-181a and lower miR-203, both of which were correlated with SLE activity. Expression levels of miR-181a and miR-203 were correlated with erythrocyte sedimentation rate, C reactive protein, anti-dsDNA antibody, complements, and SLEDAI score. Their expression levels had certain values in the differential diagnosis for active SLE (AUC=0.885 and 0.843). PFS in miR-181a high-expression individuals was lower than that in the low-miR-181 group (χ2=7.474, p=0.029). Whilst, miR-203 high-expression SLE patients had higher PFS than low-expression group (χ2=4.367, p=0.037).
Conclusions: SLE patients had higher miR-181a and lower miR-203 expression, which thus may have critical implications in disease diagnosis and evaluation.