Tsuchiya N, Williams R C
Department of Medicine and Physical Therapy, University of Tokyo School of Medicine, Japan.
West J Med. 1992 Aug;157(2):133-8.
A number of observations support molecular mimicry as a possible pathogenetic mechanism in diseases such as acute rheumatic fever, reactive arthritis after enteric infection or associated with Reiter's syndrome, myasthenia gravis, or even in rheumatoid arthritis. Molecular mimicry can be defined as a sharing of epitopes in linear or 3-dimensional presentation on disparate proteins from entirely different sources--for instance, group A streptococcal membranes and human cardiac myosin. How exposure to or infection with organisms sharing molecular similarity with antigens of the human host can evade tolerance and actually induce a self-reacting humoral or cellular immune response is still not clear; however, a large body of evidence has now been accumulated that documents apparent molecular mimicry mechanisms in these disorders. In some diseases, the molecular mimicry appears to involve human target organs and specific components of the infectious organism, whereas in others the host HLA cell surface molecules appear to share antigens with presumed bacterial or viral initiators of disease.
许多观察结果支持分子模拟作为急性风湿热、肠道感染后或与赖特综合征相关的反应性关节炎、重症肌无力甚至类风湿性关节炎等疾病可能的发病机制。分子模拟可定义为来自完全不同来源的不同蛋白质在一级结构或三维结构上存在表位共享，例如A组链球菌细胞膜与人心脏肌球蛋白。接触或感染与人类宿主抗原具有分子相似性的生物体如何逃避免疫耐受并实际诱导自身反应性体液或细胞免疫反应仍不清楚；然而，现在已经积累了大量证据，证明这些疾病中存在明显的分子模拟机制。在某些疾病中，分子模拟似乎涉及人类靶器官和感染生物体的特定成分，而在其他疾病中，宿主HLA细胞表面分子似乎与推测的疾病细菌或病毒引发剂共享抗原。
