Classical swine fever virus suppresses maturation and modulates functions of monocyte-derived dendritic cells without activating nuclear factor kappa B

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• 作者：Li-Jun Chen¹ ; Xiao-Ying Dong¹ ; Hai-Yan Shen ; Ming-Qiu Zhao ; Chun-Mei Ju ; Lin Yi ; Xue-Tao Zhang ; Yan-Mei Kang ; Jin-Ding Chen ; ^{jdchen@scau.edu.cn}
• 关键词：CSFV ; Dendritic cells ; NF-魏B ; Co-stimulatory molecule ; Cytokine
• 刊名：Research in Veterinary Science
• 出版年：2012
• 期刊代码：272_00345288
• 类别：med
• 出版时间：August, 2012
• 卷：93
• 期：1
• 页码：529-537
• 文件大小：1191 K

摘要

Classical swine fever virus (CSFV) compromises the host immune system, causing the severe disease of pigs. Dendritic cells (DCs) are the most potent inducers of immune responses. In the present study, we investigated the functional properties of porcine monocyte-derived DCs (Mo-DCs) affected by CSFV. Results showed that the expression of surface markers of DCs such as major histocompatibility complex class II (MHC-II), CD80, CD83 and CD86 were unimpaired, but an obviously increased expression of CD172a in DCs was noticed 48 h after CSFV infection. The expression profiles of cytokines were detected in cultured Mo-DCs after various treatments for 48 h by Q-RT-PCR. The findings suggested that CSFV infection significantly increased the mRNA expression of IL-10 and TNF-伪, and inhibited IL-12 expression, with little effect on IFN-伪 and IFN-纬 expression. We further demonstrated that CSFV was incapable of activating the nuclear factor kappa B (NF-魏B) in infected DCs, which was characterized by an unvaried DNA binding activity of NF-魏B, the lack of translocation of p65/RelA from the cytoplasm to the nucleus and the stabilization of p65/RelA expression. Furthermore, Western blot analysis indicated that the inactivation of NF-魏B was due to the failure of I魏B伪 degradation. The data demonstrated that CSFV could be replicated in DCs and CSFV infection could modulate the secretion of crucial co-stimulatory molecules and cytokines which down-regulated maturation of DCs, without activating NF-魏B in DCs. Thus, the results suggested a possible mechanism for CSFV evasion of innate host defenses, providing the basis for understanding molecular pathways in CSFV pathogenesis.