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自然杀伤细胞在急性肾损伤中的作用的最新进展。

Recent Advances in the Role of Natural Killer Cells in Acute Kidney Injury.

机构信息

Laboratory of Clinical and Experimental Immunology, Integrated Department of Services and Laboratories, IRCCS Istituto Giannina Gaslini, Genoa, Italy.

Department of Experimental Medicine (DIMES) and Center of Excellence for Biomedical Research (CEBR), University of Genoa, Genoa, Italy.

出版信息

Front Immunol. 2020 Aug 4;11:1484. doi: 10.3389/fimmu.2020.01484. eCollection 2020.

Abstract

Growing evidence is revealing a central role for natural killer (NK) cells, cytotoxic cells belonging to the broad family of innate lymphoid cells (ILCs), in acute and chronic forms of renal disease. NK cell effector functions include both the recognition and elimination of virus-infected and tumor cells and the capability of sensing pathogens through Toll-like receptor (TLR) engagement. Notably, they also display immune regulatory properties, exerted thanks to their ability to secrete cytokines/chemokines and to establish interactions with different innate and adaptive immune cells. Therefore, because of their multiple functions, NK cells may have a major pathogenic role in acute kidney injury (AKI), and a better understanding of the molecular mechanisms driving NK cell activation in AKI and their downstream interactions with intrinsic renal cells and infiltrating immune cells could help to identify new potential biomarkers and to select clinically valuable novel therapeutic targets. In this review, we discuss the current literature regarding the potential involvement of NK cells in AKI.

摘要

越来越多的证据表明,自然杀伤 (NK) 细胞——先天淋巴细胞 (ILC) 大家族中的细胞毒性细胞——在急性和慢性肾脏疾病中发挥着核心作用。NK 细胞的效应功能包括识别和消除病毒感染和肿瘤细胞,以及通过 Toll 样受体 (TLR) 结合感知病原体的能力。值得注意的是,它们还具有免疫调节特性,这要归功于它们分泌细胞因子/趋化因子的能力,以及与不同的先天和适应性免疫细胞建立相互作用的能力。因此,由于它们的多种功能,NK 细胞在急性肾损伤 (AKI) 中可能具有主要的致病作用,更好地了解驱动 AKI 中 NK 细胞激活的分子机制及其与内在肾细胞和浸润免疫细胞的下游相互作用,有助于识别新的潜在生物标志物,并选择具有临床价值的新型治疗靶点。在这篇综述中,我们讨论了 NK 细胞在 AKI 中潜在作用的现有文献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8d8/7438947/581002a5ebc8/fimmu-11-01484-g0001.jpg

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