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2
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Blockade of tumor necrosis factor-related apoptosis-inducing ligand exacerbates type 1 diabetes in NOD mice.肿瘤坏死因子相关凋亡诱导配体的阻断会加剧非肥胖糖尿病小鼠的1型糖尿病。
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在预防胰岛移植物排斥反应中,共移植的肝星状细胞表达的 TRAIL 起着关键作用。

A critical role of TRAIL expressed on cotransplanted hepatic stellate cells in prevention of islet allograft rejection.

机构信息

Department of General Surgery, Cleveland Clinic, Cleveland, OH 44195, USA.

出版信息

Microsurgery. 2010 May;30(4):332-7. doi: 10.1002/micr.20697.

DOI:10.1002/micr.20697
PMID:19774615
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2892209/
Abstract

Hepatic stellate cells (HSCs) have demonstrated a strong T-cell inhibitory activity. In a mouse islet transplantation model, cotransplanted HSCs can protect islet allografts from rejection. The involved mechanism is not fully understood. We showed in this study that expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), an important apoptosis-inducing ligand, on HSCs was crucial in protection of islet allografts, since HSCs derived from TRAIL knockout mice demonstrated less inhibitory activity towards T-cell proliferative responses, and substantially lost their capacity in protecting cotransplanted islet allografts from rejection, suggesting that TRAIL-mediated T cell apoptotic death is important in HSC-delivered immune regulation activity.

摘要

肝星状细胞 (HSCs) 表现出很强的 T 细胞抑制活性。在小鼠胰岛移植模型中,共移植 HSCs 可保护胰岛同种异体移植物免受排斥。其涉及的机制尚不完全清楚。在本研究中我们表明,HSCs 上表达肿瘤坏死因子相关凋亡诱导配体 (TRAIL),作为一种重要的凋亡诱导配体,对于保护胰岛同种异体移植物至关重要,因为源自 TRAIL 敲除小鼠的 HSCs 对 T 细胞增殖反应的抑制活性较弱,并且显著丧失了保护共移植胰岛同种异体移植物免受排斥的能力,提示 TRAIL 介导的 T 细胞凋亡死亡在 HSC 介导的免疫调节活性中很重要。