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巨细胞通过CXCL12/DPP4轴在狼性炎的发病过程中与中细胞进行通信

Weiwei Li¹, Chun Yao², Haixia Guo¹

¹Department of Rheumatology, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, Jiangsu, China.

Cell death & disease

|May 18, 2024

概括

这项研究表明,用林格利普丁准CXCL12/DPP4轴可以治疗狼性炎 (LN). 这种方法抑制了中细胞的增殖,并减少了LN的损伤.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
免疫学免疫学免疫学
基因组学就是基因组学.

背景情况:

狼性炎 (LN) 是系统性红斑狼 (SLE) 的严重并发症,影响50%的患者.
中细胞 (MCs) 在功能中起着至关重要的作用,在LN中可以变得过度增殖.
众所周知,炎症细胞会激活MCs,从而导致LN的损伤.

研究的目的:

用单核RNA测序来描述LN中的细胞异质性.
研究LN中巨细胞和MC之间的相互作用.
评估在LN中准CXCL12/DPP4轴的治疗潜力.

主要方法:

来自LN小鼠的细胞的单核RNA测序 (snRNA-seq).
在实验室中与巨细胞和MCs进行共同培养实验.
在体内治疗LN小鼠用linagliptin,一个DPP4抑制剂.

主要成果:

snRNA-seq发现了巨细胞和MCs之间通过CXCL12/DPP4轴介导的新型相互作用.
在实验室中,巨细胞被证明可以通过这种轴调节MC的增殖和迁移.
在LN小鼠中,林格利普丁治疗抑制了MC增殖和减少蛋白尿.

结论:

CXCL12/DPP4轴是LCN中MC功能障碍的关键调解器.
针对CXCL12/DPP4轴用linagliptin是一个有前途的治疗策略,用于LN.
这项研究为LN治疗提供了新的细胞和分子基础.

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