炎性肌病患者的再生肌纤维表达MHC-I/II分子并具备抗原呈递功能，能主动参与肌内炎症反应。我们的前期研究却发现，小鼠急性肌损伤时，罕有肌纤维表达MHC分子。这提示，不同于慢性病理损伤，急性损伤时再生肌纤维MHC表达被抑制，缺乏针对肌细胞的自身免疫。本项目将体外培养C2C12细胞、小鼠和人的原代成肌细胞并进行炎性刺激，分析成肌细胞/分化肌管的免疫特性和T细胞激活效应、以及TGF-B2，NO，NLRP3炎症小体对肌细胞免疫特性的干扰效应。制备SM-OVA Tg小鼠急性肌损伤模型并诱导肌内MHC-I/II过表达，或化学干扰TGF-B2和NO体内水平; OT细胞获得性转移。分析再生肌纤维的免疫特性、OT细胞肌内渗出、炎症小体活性改变。通过上述研究, 明确炎性刺激能否诱导肌细胞转化为免疫细胞并表达MHC和共刺激分子，分析急性损伤后抑制肌纤维免疫特性的可能原因，为骨骼肌的免疫耐受机制提供新线索。

In vivo, under physiological conditions, neither MHC I nor MHC II antigens are detectable on normal mature muscle fibers, although MHC class I and/or II was observed in muscle tissue of patients with idiopathic inflammatory myopathies. Recently, we prepared acute myoinjury mice model using different ways (Notexin/Cardiotoxin i.m., or Crush). Unexpectedly, we found MHC-Class I Expression in regenerated myofiber is rather occasional, corresponding with that, is the rarely detected CD8+ T cell in injuried muscle tissue. It implies that, inflammatory condition induced by acute-myoinjury is completely different to that in chronic-pathologic inflammation conditions, and MHC expression in acute damage induced-regenerated myofibers is blocked. This leads to the following questions: i) Whether normal muscle cells（myoblasts and myotubes）have ability to function as immune cells in the inflammatory environment? ii) Why muscle cells don’t express MHC molecules in acute muscle inflammatory condition? and which factors involved in the inhibition of immune features of muscle cells.. In this program, C2C12 cells, primary mice and human myoblasts will be cultured, differentiated, and stimulated with IFN-，LPS，Alum，or CFA. Immunologic features of myoblasts/myotubes, including the expression of MHC-I/MHC-II and co-stimulatory molecules, the production of immunorelevant cytokines, adhesion molecule and chemokines, the formation of NLRP3 inflammasomes, and the effects of muscle cells on T cell activation, will be detected and analyzed. For exploring the effects of TGF-2，NO and NLRP3 inflammasomes on immunologic features of myoblasts/myotubes, cultured cells will be imposed with chemical interference, or lentivirus transfer. In vivo study will be performed using SM-OVA Tg mice received TA muscle damage, MHC gene over-expression or not, and finally OT-I/II cell transfer. The intramuscular infiltration of OT-I/II cells, MHC expression and NLRP3 inflammasomes formation in new myofibers will be analyzed.