| Idiopathic inflammatory myopathy(IIM)is a group of clinical heterogeneous diseases characterized by skeletal muscle involvement.The pathogenesis of IIM is unknown.At present,IIM is considered to be an autoimmune disease caused by immune regulation imbalance.Clinicopathological study showed that inflammatory cell infiltration was significant in muscle tissue of IIM patients,and there was abnormal expression of pro-inflammatory helper T cell 17(Th17)and anti-inflammatory regulatory T cell(Treg),suggesting that the break of balance between the two may be an important pathogenic factor of IIM.Micro RNA is a kind of endogenous small molecule RNA,which plays an important role in maintaining the homeostasis of the immune system.Mi R-21 is up-regulated in the muscle tissue of patients with polymyositis,and glucocorticoid may regulate its expression.In order to learn more about the pathogenesis of inflammatory myopathy and explore new ways of treatment,this study combined with related signal pathways,established the experimental autoimmune myositis(EAM)mouse model,used flow cytometry,RT-PCR and other technologies to determine the expression of Th17/Treg and miR-21,and explored whether Th17/Treg immune imbalance is involved to explore the relationship between the expression of miR-21 and the proportion of Th17/Treg cells in EAM mice,and to investigate the effect of glucocorticoid treatment on the expression level of miR-21and the proportion of Th17/Treg cells.Results:the weight of mice was 17.21±0.85g in the control group and 17.44±0.77g in the EAM model group before immunization(P>0.05).After immunization,24.35±1.49g in control group,21.04±1.55g in EAM group,21.12±0.76g in hormone group(P>0.05 in hormone group and EAM group,P≤0.05 in other groups);clinical symptom score:0.00±0.00 in control group,2.44±0.50 in EAM group,1.69±0.75 in hormone group(among groups P≤0.05);muscle strength:more than 3600s in control group,79.94±26.85s in EAM group,260.32±18.23s in hormone group(among groups P≤0.05),histological score:0.19±0.26 in control group,3.19±0.70 in EAM group,1.94±0.73 in hormone group(among groups P≤0.05);the percentage of CD4~+IL-17F~+Th17s in the whole blood of mice in each group in CD4~+T cells,0.81±0.05 in control group,3.93±2.53 in EAM group,0.47±0.12 in hormone group(P>0.05 in control group and hormone group,P≤0.05 in other groups);the percentage of CD4~+CD25~+Foxp3~+Tregs in the whole blood of mice in each group in CD4~+T cells was 10.05±0.77 in the control group,7.44±1.35 in the EAM group and 16.38±3.94 in the hormone group(among groups P≤0.05);the relative expression of miR-21 in the skeletal muscle of mice was 1.23±0.87 in the control group,19.99±13.18 in the EAM group and 5.91±5.19 in the hormone group(P>0.05 in the control group and the hormone group,P≤0.05 in the other groups).Conclusion:1.The increase of the proportion of Th17 and the decrease of Treg in whole blood of EAM mice suggest that the imbalance of Th17/Treg may be involved in the pathogenesis of inflammatory myopathy.2.The expression of miR-21 in EAM group was significantly higher than that in normal control group,and the expression of Th17 cells was increased beside with Treg cells was decreased.The increase of miR-21 expression in EAM group may be mediated by negative feedback mechanism.3.The level of miR-21 in hormone group was lower than EAM group,but still higher than control group.The expression of Th17 decreased and Treg cells increased significantly in EAM mice after hormone treatment,which is to say,the immune imbalance of Th17/Treg in hormone group was improved.The pathological HE staining of skeletal muscle showed that the infiltration of inflammatory cells in muscle fibers in hormone group was significantly improved,and the decreased miR-21 may be caused by the consumption of anti-inflammatory pathway of glucocorticoid,suggesting that glucocorticoid may improve the imbalance of Th17/Treg cells through targeted regulation of miR-21 plays its therapeutic role. |
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