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产生IL-35的B细胞是自身免疫和传染病期间免疫的关键调节者
Ping Shen1, Toralf Roch1, Vicky Lampropoulou1
1Deutsches Rheuma-Forschungszentrum, a Leibniz Institute, Charitéplatz 1, 10117 Berlin, Germany.
产生互白素-35 (IL-35) 的B细胞对于免疫调节至关重要. 它们的缺失会损害自身免疫性疾病的恢复,但会增强对细菌感染的抵抗力,揭示IL-35作为治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- B 淋巴细胞通过细胞因子的产生调节免疫反应.
- 众所周知,来自B细胞的干白素-10 (IL-10) 抑制了自身免疫力,但增加了病原体的敏感性.
- 其他B细胞衍生细胞因子在免疫调节中的作用需要进一步阐明.
研究的目的:
- 调查B细胞产生的互白素-35 (IL-35) 在调节免疫反应中的作用.
- 确定IL-35缺乏B细胞对自身免疫性疾病和传染病模型的影响.
主要方法:
- 使用了缺乏IL-35表达的转基因小鼠,特别是在B细胞中.
- 在实验性自身免疫脑膜炎 (EAE) 和沙门氏菌 (Salmonella enterica) 血清 Typhimurium 感染模型中评估疾病严重程度和病原体清除.
- 分析了免疫细胞种群,激活标记物和细胞因子概况.
主要成果:
- 缺乏B细胞衍生IL-35的小鼠显示EAE恢复受损,但增强了对沙门氏菌感染的抵抗力.
- 缺少IL-35导致巨细胞和T细胞活化增加,并改善了B细胞抗原呈现细胞功能.
- IL-35和IL-10的产生主要与不同的血细胞子集有关.
结论:
- B细胞衍生的IL-35在免疫的负调节中起着至关重要的作用.
- 产生IL-35的B细胞对于控制像EAE这样的自身免疫性疾病很重要.
- 针对B细胞的IL-35产生,为自身免疫和传染病提供了潜在的治疗策略.
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