Marek’s disease virus may interfere with T cell immunity by TLR3 signals

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• 作者：Xuming Hu (1) (2)
  Wencai Xu (2)
  Aijian Qin (1) (2) (3)
  Genghua Wu (2)
  Kun Qian (1) (2) (3)
  Hongxia Shao (1) (2) (3)
  Jianqiang Ye (1) (3)
  
• 关键词：Marek’s disease virus ; Toll ; like receptor ; Chicken
• 刊名：Veterinary Research Communications
• 出版年：2014
• 出版时间：June 2014
• 年：2014
• 卷：38
• 期：2
• 页码：149-156
• 全文大小：
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• 作者单位：Xuming Hu (1) (2)
  Wencai Xu (2)
  Aijian Qin (1) (2) (3)
  Genghua Wu (2)
  Kun Qian (1) (2) (3)
  Hongxia Shao (1) (2) (3)
  Jianqiang Ye (1) (3)
  
  1. Key Laboratory of Jiangsu Preventive Veterinary Medicine, Yangzhou University, Yangzhou, 225009, People’s Republic of China
  2. Ministry of Education Key Lab for Avian Preventive Medicine, Yangzhou University, No.12 East Wenhui Road, Yangzhou, Jiangsu, 225009, People’s Republic of China
  3. Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, 225009, People’s Republic of China
  
• ISSN：1573-7446

文摘

Marek’s disease virus (MDV) is a highly oncogenic alpha-herpesvirus that causes T cell immune suppression and malignant lymphomas in chickens. Toll-like receptor (TLR) plays a dominant role in antiviral T cell immunity. However, it is unclear whether MDV induced T cell immunity is associated with TLR-mediated immunity. In this study, the expression of 28 host genes that are involved in TLR-mediated immunity and MHC-medicated T cell immunity was evaluated in chicken thymus at 7, 14, 21 and 28?days post-infection (dpi). Our results demonstrated that 24 host immune-related genes were upregulated during MDV infection at 7?dpi; however, the expression of most of these genes decreased at 21 and 28?dpi. Notably, a positive correlation was found between the down-regulation of CD4, CD8 and TLR3 signals but not the MyD88-dependent TLR pathway. The present study expanded our knowledge of host immune responses against MDV infection and our results might provide a clue that MDV may interfere with T cell immune response through TLR3 signals.