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循环自然杀伤细胞在皮肤急性感染时建立组织驻留，并介导对二次感染的加速效应反应。

Circulating NK cells establish tissue residency upon acute infection of skin and mediate accelerated effector responses to secondary infection.

机构信息

Würzburg Institute of Systems Immunology, Max Planck Research Group at the Julius-Maximilians-Universität Würzburg, Würzburg, Germany.

Würzburg Institute of Systems Immunology, Max Planck Research Group at the Julius-Maximilians-Universität Würzburg, Würzburg, Germany; International Max Planck Research School for Immunobiology, Epigenetics, and Metabolism (IMPRS-IEM), 79108 Freiburg, Germany; Faculty of Biology, University of Freiburg, 79104 Freiburg, Germany.

出版信息

Immunity. 2024 Jan 9;57(1):124-140.e7. doi: 10.1016/j.immuni.2023.11.018. Epub 2023 Dec 28.

DOI:10.1016/j.immuni.2023.11.018
PMID:38157853
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10783803/
Abstract

Natural killer (NK) cells are present in the circulation and can also be found residing in tissues, and these populations exhibit distinct developmental requirements and are thought to differ in terms of ontogeny. Here, we investigate whether circulating conventional NK (cNK) cells can develop into long-lived tissue-resident NK (trNK) cells following acute infections. We found that viral and bacterial infections of the skin triggered the recruitment of cNK cells and their differentiation into Tcf1CD69 trNK cells that share transcriptional similarity with CD56TCF1 NK cells in human tissues. Skin trNK cells arose from interferon (IFN)-γ-producing effector cells and required restricted expression of the transcriptional regulator Blimp1 to optimize Tcf1-dependent trNK cell formation. Upon secondary infection, trNK cells rapidly gained effector function and mediated an accelerated NK cell response. Thus, cNK cells redistribute and permanently position at sites of previous infection via a mechanism promoting tissue residency that is distinct from Hobit-dependent developmental paths of NK cells and ILC1 seeding tissues during ontogeny.

摘要

自然杀伤 (NK) 细胞存在于循环中，也可以在组织中发现，这些群体表现出不同的发育需求，并且在发生上被认为存在差异。在这里，我们研究了循环常规 NK (cNK) 细胞是否可以在急性感染后发育成长期存在的组织驻留 NK (trNK) 细胞。我们发现，皮肤的病毒和细菌感染触发了 cNK 细胞的募集，并使其分化为 Tcf1CD69 trNK 细胞，这些细胞与人类组织中的 CD56TCF1 NK 细胞具有转录相似性。皮肤 trNK 细胞来源于产生干扰素 (IFN)-γ 的效应细胞，并且需要转录调节因子 Blimp1 的受限表达来优化 Tcf1 依赖性 trNK 细胞的形成。在二次感染时，trNK 细胞迅速获得效应功能，并介导加速的 NK 细胞反应。因此，cNK 细胞通过一种不同于 Hobit 依赖性 NK 细胞发育途径和 ILC1 播种组织的机制重新分布并永久定位在先前感染的部位，从而促进组织驻留。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/cc3898ff676e/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/bd5909d1952e/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/c90fd766e872/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/2a295594f75c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/ddcb95d6110c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/dc42e65e605f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/9ac80fcd3368/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/a083f588b34e/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/cc3898ff676e/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/bd5909d1952e/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/c90fd766e872/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/2a295594f75c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/ddcb95d6110c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/dc42e65e605f/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/9ac80fcd3368/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/a083f588b34e/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4598/10783803/cc3898ff676e/gr7.jpg

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