PCV2诱导的内皮衍生IL-8影响MODCs成熟主要通过NF-κB信号通路
Mengyu Zhang1, Weicheng Xu1, Ning Yang1
1College of Animal Science and Technology, Beijing University of Agriculture, No. 7 Beinong Road, Beijing 102206, China.
Viruses
|April 27, 2024
概括
猪病毒2型 (PCV2) 感染通过影响血管内皮细胞 (VECs) 来降低猪免疫力. 感染PCV2的VECs释放IL-8,通过NF-κB通路抑制单细胞衍生的树突细胞 (MoDC) 成熟.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- 猪圈病毒2型 (PCV2) 导致猪的免疫抑制.
- 血管内皮细胞 (VEC) 是PCV2的点,对免疫调节至关重要.
- 感染PCV2的VECs产生IL-8,抑制单细胞衍生树突细胞 (MoDC) 的成熟.
研究的目的:
- 为了研究PCV2诱导的内皮IL-8信号通路.
- 阐明内皮IL-8抑制MoDC成熟的机制.
主要方法:
- 建立了MoDCs和PCV2感染的猪关节动脉内皮细胞 (PIECs) 的共同培养系统.
- 分析了与MoDC成熟相关的基因表达,重点关注NF-κB和JAK2-STAT3通路.
- 利用信号通路抑制剂 (NF-κB和JAK2-STAT3) 来评估它们对MoDC成熟和细胞因子产生的影响.
主要成果:
- 在PIEC中PCV2诱导的IL-8上调与降低的NF-κB信号 (RELA,p65,IκBα) 和MoDC中抑制的p65核转位相关.
- 在NF-κB通路的抑制下观察到MoDC成熟的抑制和IL-12/GM-CSF表达的减少.
- 抑制JAK2-STAT3通路对MoDC成熟或细胞因子产生没有显著影响.
结论:
- NF-κB信号通路对于MoDC成熟至关重要.
- PCV2诱导的内皮IL-8主要通过抑制NF-κB通路来抑制MoDC成熟.
- 这项研究揭示了PCV2诱导的免疫抑制的关键机制,包括内皮细胞和树突细胞的发育.
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