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LIGHT是一种肿瘤坏死因子样分子,它共刺激T细胞增殖,并且是树突状细胞介导的同种异体T细胞反应所必需的。

LIGHT, a TNF-like molecule, costimulates T cell proliferation and is required for dendritic cell-mediated allogeneic T cell response.

作者信息

Tamada K, Shimozaki K, Chapoval A I, Zhai Y, Su J, Chen S F, Hsieh S L, Nagata S, Ni J, Chen L

机构信息

Department of Immunology, Mayo Graduate and Medical Schools, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

J Immunol. 2000 Apr 15;164(8):4105-10. doi: 10.4049/jimmunol.164.8.4105.

Abstract

LIGHT is a recently identified member of the TNF superfamily and its receptors, herpesvirus entry mediator and lymphotoxin beta receptor, are found in T cells and stromal cells. In this study, we demonstrate that LIGHT is selectively expressed on immature dendritic cells (DCs) generated from human PBMCs. In contrast, LIGHT is not detectable in DCs either freshly isolated from PBMCs or rendered mature in vitro by LPS treatment. Blockade of LIGHT by its soluble receptors, lymphotoxin beta receptor-Ig or HVEM-Ig, inhibits the induction of DC-mediated primary allogeneic T cell response. Furthermore, engagement of LIGHT costimulates human T cell proliferation, amplifies the NF-kappaB signaling pathway, and preferentially induces the production of IFN-gamma, but not IL-4, in the presence of an antigenic signal. Our results suggest that LIGHT is a costimulatory molecule involved in DC-mediated cellular immune responses.

摘要

LIGHT是肿瘤坏死因子超家族最近发现的一个成员,其受体——疱疹病毒进入介质和淋巴毒素β受体,存在于T细胞和基质细胞中。在本研究中,我们证明LIGHT在源自人外周血单核细胞(PBMC)的未成熟树突状细胞(DC)上选择性表达。相比之下,无论是从PBMC中新鲜分离的DC,还是经脂多糖(LPS)处理在体外使其成熟的DC,均未检测到LIGHT。用其可溶性受体——淋巴毒素β受体-Ig或疱疹病毒进入介质-Ig阻断LIGHT,可抑制DC介导的原发性同种异体T细胞反应的诱导。此外,LIGHT的结合协同刺激人T细胞增殖,放大核因子κB信号通路,并在存在抗原信号的情况下优先诱导γ干扰素的产生,而非白细胞介素-4的产生。我们的结果表明,LIGHT是参与DC介导的细胞免疫反应的共刺激分子。

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