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白细胞介素-26 在气道宿主防御和炎症性疾病中的作用。

Interleukin-26 in host defense and inflammatory disorders of the airways.

机构信息

Unit for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, SE-17177, Sweden.

Närhälsan, Frölunda Vårdcentral, Gothenburg, SE-421 42, Sweden.

出版信息

Cytokine Growth Factor Rev. 2021 Feb;57:1-10. doi: 10.1016/j.cytogfr.2020.10.003. Epub 2020 Nov 18.

DOI:10.1016/j.cytogfr.2020.10.003
PMID:33293237
Abstract

The dimeric cytokine interleukin (IL)-26 belongs to the IL-10 family. Whereas it was originally perceived as a T-helper (Th)17 cytokine, subsequent studies have shown that IL-26 is produced by several populations of leukocytes and structural cells. This cytokine binds to a heterodimeric receptor complex including IL-10R2 and -20R1 (IL-26R) and signals through STAT 1 and 3 to induce the release of chemokines and growth factors. Remarkably, IL-26 directly kills bacteria and inhibits viral replication. The most recent studies on human airways confirm multiple cellular sources in this critical interphase of host defense and demonstrate that stimulation of toll-like receptors (TLR) trigger the release of IL-26. Once released, it exerts a dualistic effect on cytokine production and up-regulates gene expression of IL-26R. It also potentiates chemotaxis and inhibits chemokinesis for neutrophils, thereby facilitating the accumulation of innate effector cells at the site of bacterial stimulation. The high levels of IL-26 in human airways are altered in inflammatory airway disorders such as asthma and chronic obstructive pulmonary disease. Thus, IL-26 emerges as an important mediator, providing direct and indirect actions on microbes, actions that are essential for host defense and inflammation and bears potential as a biomarker of disease.

摘要

二聚体细胞因子白细胞介素(IL)-26 属于 IL-10 家族。虽然它最初被认为是辅助性 T 细胞(Th)17 细胞因子,但随后的研究表明,IL-26 由几种白细胞和结构细胞产生。该细胞因子与包括 IL-10R2 和 -20R1(IL-26R)的异二聚体受体复合物结合,并通过 STAT1 和 STAT3 信号传导诱导趋化因子和生长因子的释放。值得注意的是,IL-26 可直接杀死细菌并抑制病毒复制。最近对人类气道的研究证实了宿主防御这一关键界面中的多种细胞来源,并表明刺激 Toll 样受体(TLR)可触发 IL-26 的释放。一旦释放,它对细胞因子的产生发挥双重作用,并上调 IL-26R 的基因表达。它还增强中性粒细胞的趋化作用并抑制趋化作用,从而促进固有效应细胞在细菌刺激部位的积聚。在哮喘和慢性阻塞性肺疾病等炎症性气道疾病中,人类气道中的 IL-26 水平发生改变。因此,IL-26 作为一种重要的介质出现,对微生物具有直接和间接作用,这些作用对宿主防御和炎症至关重要,并具有作为疾病标志物的潜力。

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