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T细胞免疫球蛋白黏蛋白分子1在脓毒症发病机制中的研究进展

[Research progress of T cell immunoglobulin mucin molecule 1 in the pathogenesis of sepsis].

作者信息

Kang Shaotao, Buzukela Abuduaini, Li Yingjie, Baihetinisha Tuerdi

机构信息

Respiratory Intensive Care Unit, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830000, Xinjiang Uygur Autonomous Region, China. Corresponding author: Baihetinisha Tuerdi, Email:

出版信息

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2021 Mar;33(3):364-367. doi: 10.3760/cma.j.cn121430-20200923-00645.

DOI:10.3760/cma.j.cn121430-20200923-00645
PMID:33834983
Abstract

Sepsis 3.0 is defined as a life-threatening organ dysfunction caused by the host' uncontrol response to infection, with poor prognosis, high morbidity and fatality. Sepsis is one of the main causes of death in severe patients. As lack of comprehensive recognition of its pathogenesis, there were not specific treatment on it. It is reported that the T-cell immunoglobulin and mucin-domain-containing molecule (Tim) of Tim-1 play critical role in sepsis inflammation, immune tolerance and apoptosis, which is relative specific factor in assessment of sepsis prognostic and treatment efficiency, indicating that it could be a novel target in sepsis as well as provide a novel direction. This article mainly stated the discovery, structure, distribution and immune effect of Tim-1 as well as the possible role of TIM-1 in immunosuppression, lymphocyte proliferation and apoptosis, in order to provide reference for further research the treatment of sepsis.

摘要

脓毒症3.0被定义为由宿主对感染的失控反应引起的危及生命的器官功能障碍,预后差,发病率和死亡率高。脓毒症是重症患者主要死亡原因之一。由于对其发病机制缺乏全面认识,尚无特异性治疗方法。据报道,Tim-1家族中的T细胞免疫球蛋白黏蛋白结构域分子(Tim)在脓毒症炎症、免疫耐受及细胞凋亡中起关键作用,是评估脓毒症预后及治疗效果的相对特异性因子,提示其可能成为脓毒症治疗的新靶点并提供新方向。本文主要阐述Tim-1的发现、结构、分布、免疫效应以及TIM-1在免疫抑制、淋巴细胞增殖和凋亡中的可能作用,为进一步研究脓毒症的治疗提供参考。

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[Research progress of T cell immunoglobulin mucin molecule 1 in the pathogenesis of sepsis].T细胞免疫球蛋白黏蛋白分子1在脓毒症发病机制中的研究进展
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2021 Mar;33(3):364-367. doi: 10.3760/cma.j.cn121430-20200923-00645.
2
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Tim-3 regulates sepsis-induced immunosuppression by inhibiting the NF-κB signaling pathway in CD4 T cells.Tim-3 通过抑制 CD4 T 细胞中的 NF-κB 信号通路来调节脓毒症引起的免疫抑制。
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Blockade of the T cell immunoglobulin and mucin domain protein 3 pathway exacerbates sepsis-induced immune deviation and immunosuppression.阻断T细胞免疫球蛋白和粘蛋白结构域蛋白3通路会加剧脓毒症诱导的免疫偏离和免疫抑制。
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Immune checkpoint molecule Tim-3 promotes NKT cell apoptosis and predicts poorer prognosis in Sepsis.免疫检查点分子 Tim-3 促进 NKT 细胞凋亡,并预示脓毒症患者预后不良。
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[Study progress of role of co-suppressor molecules in sepsis immune dysfunction].共抑制分子在脓毒症免疫功能障碍中作用的研究进展
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Fragment-Based Discovery of Small Molecules Bound to T-Cell Immunoglobulin and Mucin Domain-Containing Molecule 3 (TIM-3).基于片段的小分子与 T 细胞免疫球蛋白和粘蛋白结构域包含分子 3(TIM-3)结合的发现。
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Blockade of T-cell immunoglobulin and mucin domain-containing molecule 3 aggravates T-helper cell 1 polarization in immune thrombocytopenia.阻断含T细胞免疫球蛋白和粘蛋白结构域分子3会加重免疫性血小板减少症中辅助性T细胞1极化。
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