乙肝病毒通过调控miR-21-5p/STAT3通路促进骨髓来源抑制细胞的增殖与活性OACSTPCD

Objective:To investigate the mechanism of hepatitis B virus(HBV)on myeloid-derived suppressor cells(MDSCs).Methods:C57BL/6 mice were allocated into normal and HBV groups.The chronic HBV infection model was established within the HBV group,with subsequent assessment of miR-21-5p levels in mice.Additionally,C57BL/6 mice were distributed across control,miR-21-5p negative control,miR-21-5p overexpression,and miR-21-5p knockdown groups.All mice,except those in the control group,were subjected to miR-21-5p lentiviral intervention,followed by the establishment of a chronic HBV infection mouse model.Levels of miR-21-5p and MDSCs were measured in mice.Mouse MDSCs were transfected with miR-21-5p lentivirus,exposed to HBV,and subsequent levels of p-STAT3(Ser727),Arginase-1,IL-10,and p-STAT3 proteins were assessed.Stattic was introduced into the culture medium to evaluate levels of p-STAT3,Arginase-1,and IL-10 proteins.Results:The HBV group exhibited a higher miR-21-5p expression level compared to the normal group.Compared with the control group,miR-21-5p expression levels and MDSC counts increased in the miR-21-5p negative control group,whereas both increased in the miR-21-5p overexpression group compared with the miR-21-5p knockdown group.Following the HBV infection of mouse MDSCs,there was a marked elevation in the expression of p-STAT3(Ser727),Arginase-1,IL-10,and p-STAT3 proteins.Similarly,miR-21-5p overexpression led to increased expression of p-STAT3(Ser727),Arginase-1,IL-10,and p-STAT3 proteins.Notably,upon Stattic administration,there was no discernible difference in the expression of p-STAT3,Arginase-1,and IL-10 proteins.Conclusion:HBV potentially fosters the proliferation and functional activity of MDSCs through the modulation of the miR-21-5p/STAT3 pathway.