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B细胞诱导的调节性T细胞减弱了老鼠骨髓衍生的巨细胞的经典M1极化

Yi-Ping Huang¹, Chien-Hui Chien², Li-Chieh Wang³

¹Graduate Institute of Immunology, National Taiwan University, Taipei, Taiwan.

Scientific reports

|October 10, 2025

概括

B细胞诱导的调节性T (Treg) 细胞或Treg-of-B细胞通过调节巨细胞反应有效抑制炎症. 这些Treg-of-B细胞抑制促炎标志物,促进抗炎途径,表明它们在防止过度免疫反应方面发挥作用.

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:

调节性T (Treg) 细胞对于免疫恒温至关重要.
在此之前,B细胞诱导的Treg-of-B细胞已经表现出抑制能力.
了解Treg-of-B细胞与巨细胞的相互作用是控制炎症的关键.

研究的目的:

研究Treg-of-B细胞对巨细胞的免疫调节作用.
阐明Treg-of-B细胞调节巨细胞极化和炎症反应的机制.

主要方法:

与骨髓衍生巨细胞 (BMDMs) 共同培养的Treg-of-B细胞.
对巨细胞极化标记物的基因表达 (RNA) 的分析 (Nos2,Arg1,Retnla,Mrc1,Egr2,Klf4).
测量细胞因子 (IL-10,IL-4,IL-13) 和炎症媒介 (TNF-α,IL-6,酸盐) 的产生.
研究信号通路,包括NF-κB激活和IκBα积累.

主要成果:

在刺激的巨细胞中,Treg-of-B细胞降低了M1类的炎症前导标记 (Nos2,Tnfa,Cd86,Cxcl9) 的调节,并减少了炎症媒介的产生.
在Treg-of-B细胞中,部分诱导了M2相关基因 (Arg1,Retnla,Mrc1,Egr2) 和分泌Th2细胞因子 (IL-10,IL-4,IL-13).
机制涉及细胞与细胞接触和可溶性介质,导致IκBα积累,并通过Klf4下调抑制NF-κB激活.

结论:

Treg-of-B细胞具有重要的免疫调节功能,调节巨细胞的可塑性.
这些细胞可以通过将巨细胞从促炎M1表型转移到类似M2的抗炎状态来抑制过度炎症.
在炎症性疾病中,Treg-of-B细胞是潜在的治疗点.

关键词:

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