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最近的研究提示炎症反应和异常蛋白积聚在散发性包涵体肌炎(s-IBM)的发病机制中起了重要作用。炎症反应以淋巴细胞,尤其CD8+毒性T细胞克隆扩增为特征,浸润并破坏肌纤维。慢性病毒感染触发炎症过程从而导致s-IBM的观点被第一次提出。肌纤维包涵体形成和β类淀粉物质、磷酸化tau蛋白等异常蛋白聚积是s-IBM的一个特征,可能导致内质网应激。肌纤维内病理性泛素的聚积可能同蛋白酶体功能障碍相关。炎症反应和蛋白积聚两个过程之间的关系目前仍不清楚。
Recent studies suggest that inflammatory responses and abnormal protein accumulation play an important role in the pathogenesis of sporadic inclusion body myositis (s-IBM). Inflammatory reactions are characterized by amplification of lymphocytes, especially CD8 + T-cell clones, that infiltrate and destroy muscle fibers. Chronic viral infection triggers the inflammatory process which led to s-IBM’s view being first proposed. The formation of myofibrillar inclusions and the accumulation of abnormal proteins, such as β-amyloid and phosphorylated tau, are characteristic of s-IBM and may lead to endoplasmic reticulum stress. Accumulation of pathological ubiquitin in muscle fibers may be related to proteasomal dysfunction. The relationship between the inflammatory response and protein accumulation is still unclear.