作者
Daniel L Kaufman, Michael Clare-Salzler, Jide Tian, Thomas Forsthuber, Grace SP Ting, Paul Robinson, Mark A Atkinson, Eli E Sercarz, Allan J Tobin, Paul V Lehmann
发表日期
1993/11/4
期刊
Nature
卷号
366
期号
6450
页码范围
69-72
出版商
Nature Publishing Group UK
简介
INSULIN-DEPENDENT diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice results from the T-lymphocyte-mediated destruction of the insulin-producing pancreatic β-cells and serves as a model for human IDDM1. Whereas a number of autoantibodies are associated with IDDM2, it is unclear when and to what β-cell antigens pathogenic T cells become activated during the disease process. We report here that a T-helper-1 (Thl) response to glutamate decarboxylase develops in NOD mice at the same time as the onset of insulitis. This response is initially limited to a confined region of glutamate decarboxylase, but later spreads intramolecularly to additional determinants. Subsequently, T-cell reactivity arises to other β-cell antigens, consistent with intermolecular diversification of the response. Prevention of the spontaneous anti-glutamate decarboxylase response, by tolerization of glutamate decarboxylase …
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DL Kaufman, M Clare-Salzler, J Tian, T Forsthuber… - Nature, 1993