Kohsaka Hitoshi
Department of Medicine and Rheumatology, Graduate School, Tokyo Medical and Dental University.
Nihon Rinsho. 2009 Mar;67(3):523-8.
Past paradigm that the muscle tissue injury is driven by CD4 T cells and associated humoral immunity in dermatomyositis (DM), and by cytotoxic T cells in polymyositis (PM) is now under challenge. Although pathogenic autoantigens are to be identified, skeletal muscle C-protein was an excellent immunogen to provoke experimental myositis mimicking human PM. Serum antibodies against aminoacyl tRNA synthases appear in PM/DM patients, but more often in interstitial pneumonitis patients. Inflammatory cytokines are obviously involved in the pathogenesis. Animal studies showed that autoimmune myositis occurs without tumor necrosis factor alpha. Indeed, its blockade has yielded inconsistent outcome. Most crucial ones will be therapeutic targets in the future.
过去认为，皮肌炎（DM）中肌肉组织损伤由CD4 T细胞及相关体液免疫驱动，多发性肌炎（PM）中由细胞毒性T细胞驱动，这一范式如今受到挑战。尽管致病自身抗原有待确定，但骨骼肌C蛋白是引发模拟人类PM的实验性肌炎的优良免疫原。抗氨酰tRNA合成酶的血清抗体出现在PM/DM患者中，但更常见于间质性肺炎患者。炎性细胞因子显然参与发病机制。动物研究表明，没有肿瘤坏死因子α也会发生自身免疫性肌炎。事实上，对其进行阻断产生的结果并不一致。其中最关键的将成为未来的治疗靶点。
