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1
Tissue-Resident T Cells and Other Resident Leukocytes.组织驻留 T 细胞和其他驻留白细胞。
Annu Rev Immunol. 2019 Apr 26;37:521-546. doi: 10.1146/annurev-immunol-042617-053214. Epub 2019 Feb 6.
2
Pulmonary antigen encounter regulates the establishment of tissue-resident CD8 memory T cells in the lung airways and parenchyma.肺部抗原的接触调节了肺气道和实质组织中驻留的 CD8 记忆 T 细胞的建立。
Mucosal Immunol. 2018 Jul;11(4):1071-1078. doi: 10.1038/s41385-018-0003-x. Epub 2018 Feb 16.
3
CCR8 Expression Defines Tissue-Resident Memory T Cells in Human Skin.CCR8 表达定义了人类皮肤中的组织驻留记忆 T 细胞。
J Immunol. 2018 Mar 1;200(5):1639-1650. doi: 10.4049/jimmunol.1701377. Epub 2018 Feb 2.
4
Influenza-specific lung-resident memory T cells are proliferative and polyfunctional and maintain diverse TCR profiles.流感特异性肺驻留记忆 T 细胞具有增殖性和多功能性,并保持多样化的 TCR 谱。
J Clin Invest. 2018 Feb 1;128(2):721-733. doi: 10.1172/JCI96957. Epub 2018 Jan 8.
5
Memory CD8 T cells mediate severe immunopathology following respiratory syncytial virus infection.记忆性 CD8 T 细胞介导呼吸道合胞病毒感染后的严重免疫病理。
PLoS Pathog. 2018 Jan 2;14(1):e1006810. doi: 10.1371/journal.ppat.1006810. eCollection 2018 Jan.
6
TCR-pMHC encounter differentially regulates transcriptomes of tissue-resident CD8 T cells.TCR-pMHC 相互作用差异调节组织驻留 CD8 T 细胞的转录组。
Eur J Immunol. 2018 Jan;48(1):128-150. doi: 10.1002/eji.201747174. Epub 2017 Sep 29.
7
Dynamics of influenza-induced lung-resident memory T cells underlie waning heterosubtypic immunity.流感诱导的肺驻留记忆T细胞动态变化是异源亚型免疫力下降的基础。
Sci Immunol. 2017 Jan 6;2(7). doi: 10.1126/sciimmunol.aag2031.
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Resident memory CD8 T cells in the upper respiratory tract prevent pulmonary influenza virus infection.上呼吸道中的驻留记忆性CD8 T细胞可预防肺部流感病毒感染。
Sci Immunol. 2017 Jun 2;2(12). doi: 10.1126/sciimmunol.aam6970.
9
SNP-mediated disruption of CTCF binding at the IFITM3 promoter is associated with risk of severe influenza in humans.单核苷酸多态性(SNP)介导的绝缘子蛋白(CTCF)在干扰素诱导跨膜蛋白3(IFITM3)启动子处结合的破坏与人类严重流感风险相关。
Nat Med. 2017 Aug;23(8):975-983. doi: 10.1038/nm.4370. Epub 2017 Jul 17.
10
TCR stimulation strength is inversely associated with establishment of functional brain-resident memory CD8 T cells during persistent viral infection.在持续性病毒感染期间,TCR刺激强度与功能性脑驻留记忆CD8 T细胞的建立呈负相关。
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TCR 信号强度对流感病毒感染期间固有记忆 T 细胞形成的影响。

The Impact of TCR Signal Strength on Resident Memory T Cell Formation during Influenza Virus Infection.

机构信息

Department of Microbiology and Immunology, University of Minnesota, Minneapolis, MN 55455.

Center for Immunology, University of Minnesota, Minneapolis, MN 55455.

出版信息

J Immunol. 2019 Aug 15;203(4):936-945. doi: 10.4049/jimmunol.1900093. Epub 2019 Jun 24.

DOI:10.4049/jimmunol.1900093
PMID:31235552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6684852/
Abstract

Resident memory T cells (T) in the lung are vital for heterologous protection against influenza A virus (IAV). Environmental factors are necessary to establish lung T; however, the role of T cell-intrinsic factors like TCR signal strength have not been elucidated. In this study, we investigated the impact of TCR signal strength on the generation and maintenance of lung T after IAV infection. We inserted high- and low-affinity OT-I epitopes into IAV and infected mice after transfer of OT-I T cells. We uncovered a bias in T formation in the lung elicited by lower affinity TCR stimulation. TCR affinity did not impact the overall phenotype or long-term maintenance of lung T Overall, these findings demonstrate that T formation is negatively correlated with increased TCR signal strength. Lower affinity cells may have an advantage in forming T to ensure diversity in the Ag-specific repertoire in tissues.

摘要

肺部的驻留记忆 T 细胞(T)对于异源保护流感 A 病毒(IAV)至关重要。环境因素对于建立肺部 T 细胞是必需的;然而,T 细胞内在因素(如 TCR 信号强度)的作用尚未阐明。在这项研究中,我们研究了 TCR 信号强度对 IAV 感染后肺部 T 细胞的产生和维持的影响。我们将高亲和性和低亲和性 OT-I 表位插入 IAV 中,并在 OT-I T 细胞转移后感染小鼠。我们发现,较低亲和性 TCR 刺激引起的 T 细胞形成存在偏向。TCR 亲和力并不影响肺 T 细胞的总体表型或长期维持。总的来说,这些发现表明 T 细胞的形成与 TCR 信号强度的增加呈负相关。较低亲和力的细胞可能在形成 T 细胞方面具有优势,以确保组织中抗原特异性库的多样性。