| Literature DB >> 33708193 |
Fu Long Nan1,2, Wei Zheng3, Wen Long Nan4, Tong Yu2,5, Chang Zhan Xie2, He Zhang2, Xiao Hong Xu1, Cheng Hui Li2, Zhuo Ha2, Jin Yong Zhang2, Xin Yu Zhuang2, Ji Cheng Han2,6, Wei Wang2, Jing Qian7, Guan Yu Zhao1,2, Zhuo Xin Li2, Jin Ying Ge8, Zhi Gao Bu8, Ying Zhang1, Hui Jun Lu2, Ning Yi Jin1,2.
Abstract
Newcastle disease virus (NDV) infects poultry and antagonizes host immunity via several mechanisms. Dendritic cells (DCs) are characterized as specialized antigen presenting cells, bridging innate and adaptive immunity and regulating host resistance to viral invasion. However, there is little specific knowledge of the role of DCs in NDV infection. In this study, the representative NDV lentogenic strain LaSota was used to explore whether murine bone marrow derived DCs mature following infection. We examined surface molecule expression and cytokine release from DCs as well as proliferation and activation of T cells in vivo and in vitro in the context of NDV. The results demonstrated that infection with lentogenic strain LaSota induced a phenotypic maturation of immature DCs (imDCs), which actually led to curtailed T cell responses. Upon infection, the phenotypic maturation of DCs was reflected by markedly enhanced MHC and costimulatory molecule expression and secretion of proinflammatory cytokines. Nevertheless, NDV-infected DCs produced the anti-inflammatory cytokine IL-10 and attenuated T cell proliferation, inducing Th2-biased responses. Therefore, our study reveals a novel understanding that DCs are phenotypically mature but dysfunctional in priming T cell responses during NDV infection.Entities:
Keywords: Newcastle disease virus; antigen presentation; dendritic cells; immunosuppression; phenotypic maturation; proliferation of T cells
Year: 2021 PMID: 33708193 PMCID: PMC7942023 DOI: 10.3389/fimmu.2020.619829
Source DB: PubMed Journal: Front Immunol ISSN: 1664-3224 Impact factor: 7.561