缺血性中风中的 IL-33:大脑与外周

IF 5.4 2区 医学 Q2 CELL BIOLOGY Inflammation Pub Date : 2024-09-19 DOI:10.1007/s10753-024-02148-6
Khiany Mathias, Richard Simon Machado, Anita dal Bó Tiscoski, David dos Santos, Fabricio Weinheimer Lippert, Maiara Aguiar Costa, Cinara Ludvig Gonçalves, Jaqueline Silva Generoso, Josiane Somariva Prophiro, Amanda Della Giustina, Fabricia Petronilho
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引用次数: 0

摘要

脑血管疾病是导致全球死亡和残疾的第二大原因,而中风是最常见的原因。缺血性中风时,几个过程共同产生免疫抑制,使中风后的机体容易受到感染,进而影响神经炎症。白细胞介素-33(IL-33)是白细胞介素-1 家族(IL-1)的成员之一,具有调节免疫反应和炎症的功能,在免疫反应的建立中起着至关重要的作用。研究表明,IL-33 对脑损伤有保护作用,是调节炎症细胞因子和刺激免疫调节细胞的潜在靶点。本综述以临床前和临床研究为重点,涵盖了 IL-33 对缺血性中风后免疫系统机制的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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IL-33 in Ischemic Stroke: Brain vs. Periphery

Cerebrovascular disease is the second-leading cause of death and disability worldwide, with stroke being the most common cause. In ischemic stroke, several processes combine to produce immunosuppression, leaving the post-stroke body susceptible to infection, which in turn affects neuroinflammation. Interleukin-33 (IL-33), a member of the interleukin-1 family (IL-1), functions as a modulator of immune responses and inflammation, playing a crucial role in the establishment of immunologic responses. IL-33 has been shown to have a protective effect on brain injury and represents a potential target by modulating inflammatory cytokines and stimulating immune regulatory cells. With an emphasis on preclinical and clinical studies, this review covers the impact of IL-33 on immune system mechanisms following ischemic stroke.

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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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