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胰岛特异性T细胞克隆可将糖尿病转移至非肥胖糖尿病(NOD)F1小鼠。

Islet-specific T cell clones transfer diabetes to nonobese diabetic (NOD) F1 mice.

作者信息

Peterson J D, Pike B, McDuffie M, Haskins K

机构信息

Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver 80262.

出版信息

J Immunol. 1994 Sep 15;153(6):2800-6.

PMID:8077683
Abstract

To investigate diabetes resistance to T cell-mediated disease transfer, we administered islet-specific T cell clones to the F1 progeny of nonobese diabetic (NOD) mice that were crossed with various nondiabetes-prone inbred mouse strains. We investigated four diabetogenic CD4+ T cell clones and all induced insulitis and full development of diabetes in (SWR x NOD)F1, (SJL x NOD)F1, and (C57BL/6 x NOD)F1 mice. In contrast, (BALB/c x NOD)F1 and (CBA x NOD)F1 mice were susceptible to disease transfer by some T cell clones but not others, and (C57/L x NOD)F1 mice seemed to be resistant to both insulitis and disease transfer by all of the clones tested. Disease induced by the T cell clones in susceptible F1 strains was age dependent and could only be observed in recipients younger than 13 days old. Full or partial disease resistance did not correlate with the presence or absence of I-E, different levels of Ag expression in islet cells, or differences in APC function. The results from this study suggest that there may be multiple factors contributing to susceptibility of F1 mice to T cell clone-mediated induction of diabetes, including non-MHC-related genetic background, the immunologic maturity of the recipient, and individual characteristics of the T cell clones.

摘要

为了研究糖尿病对T细胞介导的疾病转移的抗性,我们将胰岛特异性T细胞克隆注射到与各种非糖尿病易感性近交系小鼠品系杂交的非肥胖糖尿病(NOD)小鼠的F1后代中。我们研究了四种致糖尿病的CD4 + T细胞克隆,所有这些克隆均在(SWR×NOD)F1、(SJL×NOD)F1和(C57BL / 6×NOD)F1小鼠中诱导了胰岛炎和糖尿病的完全发展。相比之下,(BALB / c×NOD)F1和(CBA×NOD)F1小鼠对某些T细胞克隆的疾病转移敏感,但对其他克隆不敏感,并且(C57 / L×NOD)F1小鼠似乎对所有测试克隆的胰岛炎和疾病转移均具有抗性。T细胞克隆在易感F1品系中诱导的疾病与年龄有关,并且只能在13日龄以下的受体中观察到。完全或部分疾病抗性与I-E的存在与否、胰岛细胞中不同水平的Ag表达或APC功能的差异无关。这项研究的结果表明,可能有多种因素导致F1小鼠对T细胞克隆介导的糖尿病诱导易感,包括非MHC相关的遗传背景、受体的免疫成熟度以及T细胞克隆的个体特征。

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