外源性热冲击蛋白HSPA1A和HSPB1调节单细胞细胞的TNF-α,IL-1β和IL-10分泌
Emmanuel Ogbodo1, Francesco Michelangeli2, John H H Williams3
1Coventry University, UK.
FEBS open bio
|August 16, 2023
概括
外源热冲击蛋白 (HSP) 直接激活免疫细胞,刺激细胞因子分泌,独立于脂多糖 (LPS) 污染. 这些HSP与免疫受体相互作用,影响炎症反应.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 内源性热冲击蛋白 (HSP) 在应激细胞释放时起到危险信号的作用,可能触发诸如细胞因子分泌等免疫反应.
- 外源性HSP在免疫激活中的作用受到辩论,有建议认为脂多糖化物 (LPS) 污染可能导致观察到的效应.
研究的目的:
- 研究外源HSPA1A和HSPB1对免疫细胞激活和随后的细胞因子分泌的直接影响.
- 为了确定外源性HSP是否可以独立诱导细胞因子分泌,独立于LPS污染.
主要方法:
- 用外源HSPA1A或HSPB1.1.对U937细胞 (原始和分化的) 和外周血液单核细胞 (PBMC) 进行治疗.
- 使用ELISA测量分泌的细胞因子 (IL-1β,TNF-α,IL-10).
- 分析HSP与细胞外受体蛋白之间的相互作用 (CD14,CD36,CD11b).
主要成果:
- 无论是HSPA1A还是HSPB1,都诱导了从原始U937细胞中分泌IL-10的剂量依赖性增加.
- 差异化U937细胞和PBMCs在对外源性HSP的反应中显示出IL-1β,TNF-α和IL-10的剂量依赖分泌.
- 由HSP诱导的细胞因子分泌在很大程度上独立于LPS污染,并且HSP被证明与CD14,CD36和CD11b相互作用.
结论:
- 外源的HSPA1A和HSPB1直接激活免疫细胞,导致显著的细胞因子分泌.
- 外源性HSP的免疫激活作用不仅仅是由于LPS污染.
- CD14在对外源性HSP的反应中调解IL-1β,TNF-α和IL-10的分泌中起作用.
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