ASFV激活了STAT3,从而诱导了前病毒的M2巨细胞极化
Yanru Chen1, Haowei Chen1, Weijia Zhang1
1State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China; Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, China; Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture of the People's Republic of China, Wuhan, China; International Research Center for Animal Disease, Ministry of Science and Technology of the People's Republic of China, Wuhan, China; Hubei Jiangxia Laboratory, Wuhan, China.
非洲猪瘟病毒 (ASFV) 通过STAT3促进M2巨分化,损害免疫反应. 抑制STAT3可以减少ASFV的复制,并恢复免疫细胞功能,提供治疗见解.
科学领域:
- 兽医病毒学 兽医病毒学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 非洲猪瘟 (ASF) 是一种高度传染性的病毒性疾病,影响着全球猪业.
- 巨细胞是非洲猪瘟病毒 (ASFV) 的关键目标,但它们在感染期间的两极分化尚不清楚.
研究的目的:
- 在ASFV感染期间调查巨细胞表型变化.
- 阐明STAT3在ASFV引起的巨细胞极化中的作用.
- 评估M2极化对病毒复制和适应性免疫的影响.
主要方法:
- 在感染ASFV的猪中观察周围血液单细胞.
- 在体外巨细胞极化试验.
- 使用STATTIC.使用STAT3抑制.
- 与T细胞共同培养实验 (MLR系统).
主要成果:
- ASFV感染增加了M2单细胞种群.
- ASFV通过STAT3酸化诱导了M2极化.
- STAT3抑制阻断了M2极化,并抑制了ASFV的复制.
- M2巨细胞的杀伤能力降低,T细胞活化受损.
结论:
- ASFV通过STAT3信号操纵巨细胞偏向到M2表型.
- M2巨细胞有助于ASFV免疫逃避和持久性.
- 针对STAT3可能是对ASF控制的可行策略.
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