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新型基因改造小鼠为固有自然杀伤 T 细胞的发育和生理功能提供了新的见解。

New Genetically Manipulated Mice Provide Insights Into the Development and Physiological Functions of Invariant Natural Killer T Cells.

机构信息

Division of Stem Cell Cellomics, Center for Stem Cell Biology and Regenerative Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan.

Department of Neurology, The Neurological Institute of Jiangxi Province, Jiangxi Provincial People's Hospital, Nanchang, China.

出版信息

Front Immunol. 2018 Jun 14;9:1294. doi: 10.3389/fimmu.2018.01294. eCollection 2018.

Abstract

Invariant natural killer T (iNKT) cells are a unique T cell subset that exhibits characteristics of both innate immune cells and T cells. They express Vα14-Jα18 (-) as an invariant chain of the T cell receptor (TCR) and are restricted to the MHC class I-like monomorphic antigen presenting molecule CD1d. iNKT cells are known as immune regulators that bridge the innate and acquired immune systems by rapid and massive production of a wide range of cytokines, which could enable them to participate in immune responses during various disease states. Thus, -deficient mice, -deficient mice, or iNKT cell-overexpressing mice such as iNKT TCRα transgenic mice and iNKT cell cloned mice which contain a Vα14-Jα18 rearrangement in the TCRα locus are useful experimental models for the analysis of iNKT cells and . In this review, we describe the pros and cons of the various available genetically manipulated mice and summarize the insights gained from their study, including the possible roles of iNKT cells in obesity and diabetes.

摘要

不变自然杀伤 T(iNKT)细胞是一种独特的 T 细胞亚群,兼具先天免疫细胞和 T 细胞的特征。它们表达作为 T 细胞受体(TCR)不变链的 Vα14-Jα18(-),并受到 MHC 类 I 型单形抗原呈递分子 CD1d 的限制。iNKT 细胞被称为免疫调节剂,通过快速和大量产生广泛的细胞因子来桥接先天和获得性免疫系统,这使它们能够在各种疾病状态下参与免疫反应。因此,-缺陷小鼠、-缺陷小鼠或 iNKT 细胞过表达小鼠,如 iNKT TCRα 转基因小鼠和 iNKT 细胞克隆小鼠,其 TCRα 基因座中存在 Vα14-Jα18 重排,是分析 iNKT 细胞和 的有用实验模型。在这篇综述中,我们描述了各种可用的基因修饰小鼠的优缺点,并总结了从它们的研究中获得的见解,包括 iNKT 细胞在肥胖和糖尿病中的可能作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b723/6010523/cb8dbda919db/fimmu-09-01294-g001.jpg

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