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NOD T淋巴细胞中活化诱导的细胞死亡存在缺陷:1,25-二羟维生素D3可修复该缺陷。

Defective activation-induced cell death in NOD T lymphocytes: 1,25-dihydroxyvitamin D3 restores defect.

作者信息

Decallonne B, Mathieu C

机构信息

Laboratorium voor Experimentele Geneeskunde en Endocrinologie (LEGENDO), Katholieke Universiteit Leuven, Leuven, Belgium.

出版信息

Ann N Y Acad Sci. 2003 Nov;1005:176-7. doi: 10.1196/annals.1288.021.

Abstract

The aim of this study was first to analyze strain differences in apoptosis resistance of NOD peripheral T lymphocytes in in vitro models of death by neglect and activation-induced cell death (AICD). Especially AICD is known to play a key role in peripheral tolerance, keeping autoimmune effector cells under control. Second, we studied the effects of in vivo treatment of NOD mice with 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)], an immunomodulator known to prevent diabetes and insulitis in NOD mice, on in vitro T lymphocyte apoptosis resistance.

摘要

本研究的目的首先是在忽视性死亡和激活诱导的细胞死亡(AICD)的体外模型中分析NOD外周T淋巴细胞抗凋亡能力的品系差异。特别是已知AICD在外周耐受中起关键作用,可控制自身免疫效应细胞。其次,我们研究了用1α,25 - 二羟基维生素D(3) [1α,25(OH)₂D₃]对NOD小鼠进行体内治疗对体外T淋巴细胞抗凋亡能力的影响,1α,25(OH)₂D₃是一种已知可预防NOD小鼠糖尿病和胰岛炎的免疫调节剂。

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