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The Importance of the Bursa of Fabricius, B Cells and T Cells for the Pathogenesis of Marek’s Disease: A Review

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 196...

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Detalles Bibliográficos
Autor principal: Schat, Karel A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9504545/
https://www.ncbi.nlm.nih.gov/pubmed/36146821
http://dx.doi.org/10.3390/v14092015
Descripción
Sumario: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.