人类CD24+CD38+调节性B细胞通过IL-10和PD-L1的协同作用促进亲溶解的巨细胞功能
Elaheh Dalir Abdolahinia1, Elizabeth M Horta2, Takumi Memida1
1Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University, Davie, FL 33314, United States.
Journal of leukocyte biology
|October 8, 2025
概括
调控性B细胞 (CD24+CD38+) 通过IL-10和PD-L1/PD-1信号传递促进抗炎性巨细胞的分化. 这揭示了解决慢性疾病炎症的新途径.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 炎症研究 炎症研究
背景情况:
- 调节性B细胞 (CD24+CD38+) 分泌互白素10 (IL-10) 来减少炎症.
- 这些B细胞在调节巨细胞分化中的作用尚不清楚.
研究的目的:
- 研究CD24+CD38+调节性B细胞如何影响亲溶解性巨细胞的分化和功能.
- 探索涉及编程死亡-1 (PD-L1) /编程死亡-1 (PD-1) 相互作用和IL-10的机制.
主要方法:
- 隔离人类CD24+CD38+B细胞和与THP-1衍生巨细胞共同培养.
- 使用重组IL-10,PD-L1和中和抗体的功能增益和丧失研究.
- 通过流细胞计,qPCR和质谱仪分析巨细胞极化,PD-1表达,细胞和脂质媒介的产生.
主要成果:
- 共同培养显著增加了M2巨细胞的两极分化,PD-1表达和细胞.
- 抑制IL-10或PD-L1通路减少了M2巨细胞的分化和活性.
- 观察到促进溶解的脂质介质 (12-HEPE,RvD5) 的增强产生.
结论:
- 人类CD24+CD38+调节性B细胞促进巨介导炎症的解决.
- 这通过IL-10分泌和PD-L1/PD-1结合发生,突出显示了一种新的调节途径.
- 这些发现表明,慢性炎症疾病的潜在治疗点.
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