Smiley J D, Moore S E
Department of Medicine, University of Texas Health Science Center, Southwestern Medical School, Dallas.
Am J Med Sci. 1988 May;295(5):478-96. doi: 10.1097/00000441-198805000-00014.
Autoimmune diseases result from a combination of genetic susceptibility factors and exogenous influences such as infection or chemical (including drug) exposure. Germline DNA variations in genetic type as well as defects in antigen recognition acquired during thymic education of developing T-lymphocytes both contribute to impaired self: nonself discrimination and set the stage for later development of such diseases as myasthenia gravis, polymyositis, or systemic lupus erythematosus. In addition, drugs such as D-penicillamine, hydralazine, procainamide, or quinidine induce T-cell or B-cell changes which precipitate auto-reactivity and cause drug-induced disease. Intervention in autoimmune diseases with prednisone, alkylating agents or the future use of more selective monoclonal antibody reagents may be life-saving in some of these disorders.
自身免疫性疾病是由遗传易感因素和外源性影响（如感染或化学物质暴露，包括药物）共同作用导致的。遗传类型中的种系DNA变异以及发育中的T淋巴细胞在胸腺教育过程中获得的抗原识别缺陷，都导致了自身与非自身识别受损，并为重症肌无力、多发性肌炎或系统性红斑狼疮等疾病的后期发展奠定了基础。此外，D-青霉胺、肼屈嗪、普鲁卡因胺或奎尼丁等药物会引起T细胞或B细胞变化，从而引发自身反应性并导致药物性疾病。在某些自身免疫性疾病中，使用泼尼松、烷化剂进行干预，或未来使用更具选择性的单克隆抗体试剂，可能会挽救生命。
