Rose N R
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA.
Semin Immunol. 1998 Feb;10(1):5-13. doi: 10.1006/smim.1997.0100.
Autoimmune disease has long been considered a shadow following infectious diseases. Epidemiological evidence shows that rheumatic fever follows streptococcal infection and Trypanosoma cruzi infection is the instigator of Chagas' disease. There is, however, very little information of the mechanism by which such a train of events is initiated. Autoimmunity, in a form of autoantibodies, is common after many infections and may well result from the mimicking of host proteins by antigens of the infectious agent. There are, however, few if any examples in humans where molecular mimicry gives rise to autoimmune disease. The progression from benign autoimmunity to pathogenic autoimmune disease depends upon the balance of cytokines produced during the inflammatory process accompanying infection. In many autoimmune diseases, the cytokine profile favors the proinflammatory cytokines, IFN-gamma and IL-1, which support the production of disease. A searching study of cytokine profiles during infection may offer a promising approach to avoiding the harmful consequences of post-infection autoimmune responses.
自身免疫性疾病长期以来一直被视为传染病的阴影。流行病学证据表明，风湿热继发于链球菌感染，而克氏锥虫感染是恰加斯病的诱因。然而，关于引发这一系列事件的机制的信息却非常少。以自身抗体形式存在的自身免疫在许多感染后很常见，很可能是由于感染因子的抗原模拟宿主蛋白所致。然而，在人类中，分子模拟引发自身免疫性疾病的例子极少，如果有的话。从良性自身免疫发展到致病性自身免疫性疾病取决于感染伴随的炎症过程中产生的细胞因子的平衡。在许多自身免疫性疾病中，细胞因子谱有利于促炎细胞因子IFN-γ和IL-1，它们支持疾病的产生。对感染期间细胞因子谱的深入研究可能为避免感染后自身免疫反应的有害后果提供一种有前景的方法。
