Abstract
Oral lichen planus (OLP) is a T cell-mediated immune disorder, and we have indicated a Th1-dominated immune response in OLP. MicroRNA-155 (miR-155) could promote Th1 cells polarization. The present study aims to determine the role of miR-155 in immune response of OLP. The expression of miR-155 and the target mRNA was tested by Real-Time PCR. The serum levels of IL-2, 4, 10 and IFN-γ were examined with ELISA. Furthermore, in vitro study was built to observe the function of miR-155 in erosive-type OLP (EOLP). Finally, we determined the expression and correlation of miR-155 and SOCS1 in EOLP CD4+ T cells. The results showed miR-155 was high related with the disease severities. Besides, serum IFN-γ was specifically increased in EOLP group, while IL-4 was decreased. In vitro studies showed miR-155 could reinforce IFN-γ signal transducer, and the induction of IFN-γ could also promote miR-155 expression in EOLP CD4+ T cells. In addition, miR-155 levels were negatively related with SOCS1 mRNA expression in EOLP CD4+ T cells. Our study revealed a positive miR-155- IFN-γ feedback loop in EOLP CD4+ T cell, which might contribute to the Th1-dominated immune response. Furthermore, miR-155 could be used for the evaluation and treatment of OLP.
Highlights
Disorders[14,15,16,17]
The expression of miR-155 increased in peripheral blood of erosive type OLP (EOLP) patients compared with the control (p < 0 .05), in addition, the expression of miR-155 in EOLP group was significant higher than that in non-erosive type OLP (NEOLP) group (p < 0.05) (Fig. 1A)
The correlation analysis revealed that the miR-155 expression was highly related with the RAE scores which represented the severities of Oral lichen planus (OLP) (p < 0.01, r = 0.855) (Fig. 1B), and the correlation coefficient was much higher in EOLP patients (p < 0.01, r = 0.882) (Fig. 1C)
Summary
Disorders[14,15,16,17]. MiR-155 is encoded within an exon of the non-coding RNA known as B cell integration cluster (Bic) gene[17]. In many immune diseases such as multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus and inflammatory bowel disease, miR-155 was found to have abnormal expression in peripheral blood of the patients[18,19,20]. MiR-155 in activated CD4+ T cells could promote Th17 cell differentiation, and knocking out of bic gene might lead to a break of Th1/Th2 balance in CD4+ T cells[19,20,21,22]. Suppressor of cytokine signaling 1 (SOCS1) was considered as a key target of miR155 in Th1 cells, which negatively regulated JAKs-SATAT1 signaling. Our aim was to determine the expression of miR-155 in peripheral blood of OLP patients, and analyze the relationship of miR-155 with the cytokines. Through regulating miR-155 expression, observations in vitro were built to examine their effects on OLP CD4+ T cells proliferation and the levels of cytokines. Certain target of miR-155 would be predicted and confirmed
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