Benderly A, Etzioni A
Surv Immunol Res. 1985;4(4):319-24. doi: 10.1007/BF02918740.
In order to summarize all the data regarding the immunological findings in RF we have elaborated the following theory about the pathogenesis of RF (fig. 1). The disease will develop only after repeated beta-hemolytic group A streptococcal throat infection in susceptible individuals. In these people, who have a specific immune response to repeated streptococcal infection due to their DR region, a decrease in suppressor activity will develop. This will lead to an increased specific humoral and cellular immune response to streptococcal antigen which cross-reacts with specific human tissue as the heart or the brain. Alternatively or concomitantly specific autoantibodies against these tissues are made. These antibodies together with the cellular response will cause the clinical manifestation seen in RF. This is only a proposed theory and still much more work has to be done to solve the enigma regarding the pathogenesis of RF.
为了总结有关风湿热(RF)免疫学发现的所有数据,我们阐述了以下关于RF发病机制的理论(图1)。该疾病仅在易感个体反复发生A组β溶血性链球菌咽喉感染后才会发展。在这些由于其DR区域对反复的链球菌感染具有特异性免疫反应的人群中,抑制活性会降低。这将导致对链球菌抗原的特异性体液免疫和细胞免疫反应增强,而该抗原与心脏或大脑等特定人体组织发生交叉反应。另外或同时,会产生针对这些组织的特异性自身抗体。这些抗体与细胞反应一起将导致RF中出现的临床表现。这只是一个提出的理论,要解开关于RF发病机制的谜团,仍有更多工作要做。