Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Viruses. 2022 Sep 12;14(9):2015. doi: 10.3390/v14092015.
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.
自 20 世纪 60 年代末以来,法氏囊(BF)在马立克氏病(MD)发病机制中的重要性一直受到研究。在本综述中,根据鸡免疫系统发育和 MD 发病机制的现有知识,分析了这些研究的结果。基于可用于干扰 BF 发育的现有技术,确定并讨论了三个不同的时期。在 1968 年至 1977 年的最初阶段,使用新生期去法氏囊、化学方法和辐照是干扰 B 淋巴细胞发育的主要工具。这些技术的应用导致了从无影响到增加或减少 MD 发病率的结果。从 20 世纪 70 年代末开始,在 18 日龄胚胎中使用去法氏囊导致了 MD 发病机制的“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,导致胸腺衍生淋巴细胞(T 细胞)的激活。根据该模型,这些被激活的 T 细胞,而不是静止的 T 细胞,容易受到 MDV 感染和随后的转化。最后,缺乏 IgY 重链基因 J 基因片段的 B 细胞敲除鸡被用于进一步定义 BF 在 MD 发病机制中的作用。