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中性粒细胞-介质细胞轴在狼性炎中促进了淋巴细胞损伤

Norio Hanata¹, Carmelo Carmona-Rivera¹, Victoria Hoffmann²

¹Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.

Annals of the rheumatic diseases

|December 7, 2025

概括

中性细胞细胞外陷 (NETs) 通过激活细胞来驱动狼性炎 (LN),导致炎症和纤维化. 准这种NET-介质细胞轴为LN提供了潜在的治疗策略.

科学领域:

免疫学免疫学免疫学
腎臟病學 (nephrology) 是一種醫學專業.
细胞生物学细胞生物学

背景情况:

狼性炎 (LN) 是系统性红斑狼 (SLE) 的严重并发症.
关联中性粒细胞激活与LN早期损伤的精确机制尚未完全理解.
中性细胞外细胞陷 (NETs) 与自身免疫性疾病有关,但它们在LN病原发生中的作用需要进一步调查.

研究的目的:

调查中性粒细胞和NETs在LN进展期间中细胞 (MC) 激活中的作用.
阐明NETs在LN.中导致损伤的机制.
在LN的NET-介质细胞轴内识别潜在的治疗点.

主要方法:

在LN的小鼠模型中的组织学和流细胞计.
对人体LN脏活检进行NET和中性粒细胞透的分析.
在体外刺激人类MCs与NETs或素基因素H3 (citH3).
在SLE患者中,与酶相关的免疫吸收试验,RNA测序和血NET残留物 (citH3-DNA复合物) 的测量.

主要成果:

NETs积聚在LN脏的中区域,与疾病严重程度和中扩张相关.
MCs内部化了NETs,通过托尔类受体4 (TLR4) 促进了它们的增殖和激活.
激发CitH3可以调高促炎性细胞因子,I型干扰素刺激基因和MCs中的IV型原.
在活跃的LN患者中,血citH3-DNA水平升高与疾病活性和器官参与相关.

结论:

中性粒细胞透和NET形成在LN期间在中早期发生.
NET衍生的citH3通过TLR4激活MCs,促进炎症和纤维化.
一个新的NET-mesangial细胞轴被确定为LN病变发生的关键驱动因素.
这一NET-MC轴代表了狼性炎的潜在治疗点.

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