炎症性疾病中中性粒细胞与凋亡诱导配体的协同作用。

IF 4.2 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2025-03-12 eCollection Date: 2025-01-01 DOI:10.2147/JIR.S506807
Hanyu Xue, Ran Xie, Zhiwei Wang, Wenqian Fan, Yinxiang Wei, Lijie Zhang, Dan Zhao, Zhiming Song
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引用次数: 0

摘要

中性粒细胞作为最丰富的先天免疫细胞,在宿主抗感染活性和无菌炎症的组织损伤/修复过程中起着关键作用。由于受到细胞凋亡等调控机制的限制,中性粒细胞在体内的存活时间较短。由于细胞质区域存在死亡结构域,肿瘤坏死因子受体超家族(TNFRSF)的一些成员被定义为死亡受体,如tnfr - 1、Fas和DR4/DR5。TNF-α、FasL和TRAIL被称为凋亡诱导配体,它们可以与死亡受体结合,激活细胞内凋亡通路,诱导细胞凋亡。越来越多的研究发现,这三种诱导凋亡的配体通过与中性粒细胞的协调在免疫系统中发挥重要作用,包括中性粒细胞的募集/浸润和功能的执行。本文综述了目前针对中性粒细胞在疾病诊断和治疗方面的研究,重点介绍了在目前的认知下,受凋亡诱导配体调控的中性粒细胞在炎症性疾病中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Coordination of Neutrophil and Apoptosis-Inducing Ligand in Inflammatory Diseases.

As the most abundant innate immune cells, neutrophils play a key role in host's anti-infective activity and tissue damage/repair process of sterile inflammation. Due to the restriction of apoptosis and other regulatory mechanisms, neutrophils have a short survival time in vivo. Because of the death domain of cytoplasmic regions, some members of tumor necrosis factor receptor superfamily (TNFRSF) are defined as death receptors, such as TNFR-I, Fas and DR4/DR5. TNF-α, FasL and TRAIL, which are known as apoptosis-inducing ligand, can bind to death receptors and activate intracellular apoptosis pathways to induce apoptosis. Accumulating studies found that these three apoptosis-inducing ligands play an important role in the immune system by coordinating with neutrophil, which including neutrophil recruitment/infiltration and function performing. In this review, we summarize existing studies targeting neutrophils as diagnosis and treatment for diseases, and focus on the involvement of neutrophils which regulated by apoptosis-inducing ligands in inflammatory diseases under current cognition.

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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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