追踪LYVE1腹膜液巨细胞揭示了两条通往居民巨细胞重新填充的途径,它们对单细胞的依赖程度不同
Alexandre Gallerand1, Jichang Han1, Rachel L Mintz1,2,3
1Division of Immunobiology, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA.
bioRxiv : the preprint server for biology
|April 1, 2025
概括
住宿腹腔巨细胞 (大腔巨细胞,LCMs) 在受伤后通过两个不同的途径补充. 一个途径涉及单细胞和CD73-LYVE1+中间体,而另一个途径绕过了这个阶段,以更快的 Gata6+CD73+ LCM再生.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 组织再生 组织再生
背景情况:
- 常驻小鼠腹巨细胞,称为大腔巨细胞 (LCM),起源于胚胎原始体.
- 成熟的LCM表达CD73和Gata6 (CD73+Gata6+). 这两种表达的基因是CD73和Gata6.
- 传统上,单细胞被认为可以通过CD73-LYVE1+中间体在受伤后补充LCM.
研究的目的:
- 为了研究在受伤后补充居民腹膜巨细胞 (LCM) 的机制和途径.
- 为了澄清CD73-LYVE1+ LCMs在腹膜重新填充中的作用.
主要方法:
- 在小鼠身上进行命运映射研究.
- 在照射和炎症后对巨细胞群 (CD73, Gata6, LYVE1) 的分析.
- 单细胞枯竭实验. 一个细胞枯竭实验.
- 评估因特格林介导的与中皮细胞的相互作用.
主要成果:
- CD73-LYVE1+ LCMs通过与中层表面的相互作用可以分化为Gata6+CD73+ LCMs.
- 由CD73-LYVE1+ LCMs产生的腹膜再填充取决于和与单细胞招募成正比.
- 意想不到的是,受伤后仅约10%的Gata6依赖的LCM依赖于LYVE1+中间阶段.
- 即使在单细胞贫乏的条件下,LCMs也在辐射后有效地反弹,这表明了另一种途径.
结论:
- 两个平行通路有助于在炎症性损伤后补充居住腹巨细胞.
- 这些途径涉及不同的分化中间体,对单细胞的依赖程度各不相同.
- 这些发现挑战了单细胞衍生的CD73-LYVE1+中间体是LCM再生的唯一来源的独特模型.
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