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不同的ILC3对PDGF-D的反应控制了粘膜免疫

José L Fachi¹, Sarah de Oliveira^1,2, Tihana Trsan¹

¹Department of Pathology and Immunology, Washington University School of Medicine in St. Louis, Saint Louis, MO, USA.

Science immunology

|February 27, 2026

概括

血小板衍生生长因子D (PDGF-D) 通过PDGFRβ调节小鼠的先天性淋巴细胞 (ILC),促进IL-22. 相比之下,PDGF-D激活NKp44诱导IFN-γ,揭示不同的免疫感应机制.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

血小板衍生生长因子D (PDGF-D) 是人类NKp44+3组先天性淋巴细胞 (ILC3) 的非正规配体.
鼠ILC3缺乏NKp44,因此需要对小鼠的PDGF-D替代调节途径进行研究.

研究的目的:

阐明PDGF-D调节小鼠ILC3s的独特机制.
了解PDGF-D信号在粘膜免疫和宿主防御肠道感染中的作用.

主要方法:

利用PDGFRβ淘汰赛小鼠和NKp44转基因小鼠研究PDGF-D介导的ILC3反应.
评估了介质素-22 (IL-22),瘤亡因子-α和干扰素-γ (IFN-γ) 的产生.
使用PDGF-D记者小鼠进行组织定位分析.

主要成果:

在小鼠中,PDGF-D通过PDGF受体β (PDGFRβ) 促进IL-22的产生和ILC3的扩散.
在ILC3s中PDGFRβ缺乏,使人易受肠道感染.
转基因小鼠中NKp44的PDGF-D参与诱导了一种具有保护性和有害性IFN-γ生产的1型效应器程序.
在炎症期间,纤维细胞和内皮细胞被确定为PDGF-D的关键来源.

结论:

PDGF-D利用ILC3s进化上不同的感知机制,在小鼠中介于PDGFRβ,在人类中介于NKp44.
这些不同的途径在感染期间对粘膜免疫和宿主防御有不同的贡献.

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