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IL-10 产生的自然杀伤细胞在全身性感染炎症调节机制中的作用。

Role of IL-10-Producing Natural Killer Cells in the Regulatory Mechanisms of Inflammation during Systemic Infection.

机构信息

Department of Research in Biochemistry, Research Unit, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.

出版信息

Biomolecules. 2021 Dec 21;12(1):4. doi: 10.3390/biom12010004.

DOI:10.3390/biom12010004
PMID:35053151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8773486/
Abstract

Natural killer (NK) cells have the dual ability to produce pro-inflammatory (IFNγ) and anti-inflammatory (IL-10) cytokines during systemic infection, which points to their crucial role both as inflammatory effectors for infection clearance and as regulators to counterbalance inflammation to limit immune-mediated damage to the host. In particular, immunosuppressive IL-10 secretion by NK cells has been described to occur in systemic, but not local, infections as a recent immunoregulatory mechanism of inflammation that may be detrimental or beneficial, depending on the timing of release, type of disease, or the infection model. Understanding the factors that drive the production of IL-10 by NK cells and their impact during dualistic inflammatory states, such as sepsis and other non-controlled inflammatory diseases, is relevant for achieving effective therapeutic advancements. In this review, the evidence regarding the immunoregulatory role of IL-10-producing NK cells in systemic infection is summarized and discussed in detail, and the potential molecular mechanisms that drive IL-10 production by NK cells are considered.

摘要

自然杀伤 (NK) 细胞在全身感染期间具有产生促炎 (IFNγ) 和抗炎 (IL-10) 细胞因子的双重能力,这表明它们作为清除感染的炎症效应物和作为调节剂来平衡炎症以限制对宿主的免疫介导损伤的关键作用。特别是,NK 细胞的免疫抑制性 IL-10 分泌被描述为发生在全身感染中,而不是局部感染中,作为炎症的最近的免疫调节机制,其可能是有害的或有益的,这取决于释放的时间、疾病的类型或感染模型。了解驱动 NK 细胞产生 IL-10 的因素及其在败血症和其他非控制性炎症性疾病等双重炎症状态中的影响对于实现有效的治疗进展是相关的。在这篇综述中,详细总结和讨论了在全身感染中产生 IL-10 的 NK 细胞的免疫调节作用的证据,并考虑了驱动 NK 细胞产生 IL-10 的潜在分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b72b/8773486/108bb3443623/biomolecules-12-00004-g008.jpg
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