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Expression of miRNA-21 in experimental autoimmune myositis mouse after radiation and its correlation with Th17 /Treg immune imbalance
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L. Wang   , Q. Ye , W. Yan |
| Department of Neurology, Ningbo No.2 Hospital, Ningbo 315000, China , Yw961804121@163.com |
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Abstract: (12 Views) |
Background: Experimental autoimmune myositis (EAM) is characterized by immune-mediated skeletal muscle inflammation. Imbalance between Th17 and regulatory T (Treg) cells contributes to disease pathogenesis. MicroRNA-21 (miR-21) has been implicated in immune regulation and radiation responses, yet its role in EAM remains unclear. This study aimed to investigate the expression of miR-21 following local radiation in a murine EAM model and to assess its correlation with Th17/Treg immune imbalance. Materials and Methods: Female C57BL/6 mice were induced with EAM and randomized into control and radiation groups. Local hindlimb irradiation (15 Gy) was administered to the radiation group. Muscle tissues and draining lymph nodes were collected at day 28 post-induction. Flow cytometry quantified Th17 (CD4⁺IL-17A⁺) and Treg (CD4⁺FoxP3⁺) populations. Quantitative real-time PCR measured miR-21 expression in muscle samples. Correlations between miR-21 levels and Th17/Treg ratios were analyzed. Results: Radiation significantly reduced muscle inflammation and improved histopathological scores compared to non-irradiated EAM mice (p<0.05). Th17 frequencies decreased while Treg frequencies increased following irradiation (p<0.01). miR-21 expression was significantly downregulated in irradiated muscle tissues (p<0.01). Notably, miR-21 levels showed a positive correlation with Th17/Treg ratios (r=0.68, p<0.01). Conclusion: Local radiation modulates immune responses in EAM by downregulating miR-21 and restoring Th17/Treg balance, suggesting a potential therapeutic mechanism involving miR-21-mediated immune regulation. |
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| Keywords: Experimental autoimmune myositis, miR-21, Th17 cells, regulatory T-cells, immune imbalance, radiation. |
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Full-Text [PDF 946 kb]
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Type of Study: Original Research |
Subject:
Radiation Biology
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