T cell subset profile and inflammatory cytokine properties in the gut-associated lymphoid tissues of chickens during inf
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ORIGINAL ARTICLE
T cell subset profile and inflammatory cytokine properties in the gut‑associated lymphoid tissues of chickens during infectious bursal disease virus (IBDV) infection Yina Ruan1 · Yan Wang2 · Yueping Guo1 · Yiwei Xiong1 · Mianmian Chen1 · Ayong Zhao1 · Hebin Liu2 Received: 18 November 2019 / Accepted: 12 June 2020 © Springer-Verlag GmbH Austria, part of Springer Nature 2020
Abstract While infectious bursal disease virus (IBDV) mainly targets immature B cells and causes T cell infiltration in the bursa of Fabricius (BF) of chickens, the effect of IBDV infection on the properties of T cells and relevant cytokine production in avian gut-associated lymphoid tissues (GALTs) remains unknown. Here, we show that while the CD8+ T cell subset is not affected, IBDV infection decreases the percentage of C D4+ T cells in the cecal tonsil (CT), but not in esophagus tonsil, pylorus tonsil, and Meckel’s diverticulum of GALTs, in contrast to BF and spleen, in which the proportion of CD4+ cells increases upon IBDV infection. Further, IBDV infection upregulates IFN-γ, IL-10, and the T cell checkpoint receptor LAG-3 mRNA expression in BF. In contrast, in CTs, IBDV infection significantly increases the production of IFN-β and CTLA-4 mRNA, while no significant effect is seen in the case of IFN-γ, IL-10 and LAG-3. Together, our data reveal differential modulation of T cell subsets and proinflammatory cytokine production in different lymphoid tissues during the course of IBDV infection.
Introduction Infectious bursal disease virus (IBDV) is the etiologic agent of infectious bursal disease (IBD), also known as Gumboro disease, a highly contagious and immunosuppressive disease in young chickens [1–3]. IBDV mainly targets the actively dividing B cells in the bursa of Fabricius (BF), a unique primary immune organ of juvenile avian species, leading to depletion of B cells in the bursa via necrosis and apoptotic processes [4, 5]. Bursal Handling Editor: Roman Pogranichniy. Yina Ruan and Yan Wang contributed equally to this work. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00705-020-04735-y) contains supplementary material, which is available to authorized users. * Hebin Liu [email protected] 1
Department of Veterinary Medicine, College of Animal Science and Technology, Zhejiang A&F University, 600 Wusu street, Lin’an, Hangzhou, Zhejiang, China
Department of Biological Sciences, Xi’an Jiaotong-Liverpool University, 111 Ren’ai Road, SIP, Suzhou, Jiangsu 215123, China
2
edema and atrophy manifest as a major symptom of IBDV infection [2, 6]. As a consequence, IBDV infection can cause morbidity and mortality and impair the immune competence of young birds, which increases the susceptibility of chickens to other infections and compromises vaccination against other diseases [7]. In addition to mainly infecting dividing B cells in the BF, IBDV can also directly target the original immune cells in other immune organs or tissues such as thymus, spleen, bone marrow,
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