自1960年代后期以来,人们就研究了法氏囊(BF)对马立克氏病(MD)发病机理的重要性。在这次审查中,这些研究的结果是在1968年至2022年对鸡的免疫系统和MD发病机理的不断发展的知识的背景下进行分析的。基于现有的技术来干扰BF的发展,确定和讨论了三个不同的时期。在1968年至1977年之间的最初时期,使用新生儿囊切除术,化学方法和辐照是干扰B淋巴细胞发育的主要手段。这些技术的应用导致从无影响到MD发病率的增加或减少的矛盾结果。从1970年代末开始,在18天大的胚胎中使用囊切除术导致了MD发病机理的“康奈尔模型”的发展,其中B淋巴细胞的感染是MD病毒(MDV)复制的重要第一步,导致胸腺衍生的淋巴细胞(T细胞)的激活。按照这个模型,这些活化的T细胞,但不是静息的T细胞,易受MDV感染和随后的转化。最后,缺乏IgY重链基因的J基因片段的B细胞敲除鸡用于进一步确定BF在MD发病机理中的作用。
The importance of the bursa of Fabricius (BF) for the pathogenesis of Marek\'s disease (MD) has been studied since the late 1960\'s. In this
review, the results of these studies are analyzed in the context of the developing knowledge of the immune system of chickens and the pathogenesis of MD from 1968 to 2022. Based on the available techniques to interfere with the development of the BF, three distinct periods are identified and discussed. During the initial period between 1968 and 1977, the use of neonatal bursectomy, chemical methods and irradiation were the main tools to interfere with the B lymphocyte development. The application of these techniques resulted in contradictory results from no effects to an increase or decrease in MD incidence. Starting in the late 1970\'s, the use of bursectomy in 18-day-old embryos led to the development of the \"Cornell model\" for the pathogenesis of MD, in which the infection of B lymphocytes is an important first step in MD virus (MDV) replication causing the activation of thymus-derived lymphocytes (T cells). Following this model, these activated T cells, but not resting T cells, are susceptible to MDV infection and subsequent transformation. Finally, B-cell knockout chickens lacking the J gene segment of the IgY heavy chain gene were used to further define the role of the BF in the pathogenesis of MD.