Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice

被引:0
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作者
Maki Nakayama
Norio Abiru
Hiroaki Moriyama
Naru Babaya
Edwin Liu
Dongmei Miao
Liping Yu
Dale R. Wegmann
John C. Hutton
John F. Elliott
George S. Eisenbarth
机构
[1] University of Colorado Health Sciences Center,Barbara Davis Center for Childhood Diabetes
[2] Nagasaki University,Graduate School of Biomedical Sciences
[3] Kobe University Graduate School of Medicine,undefined
[4] University of Alberta,undefined
来源
Nature | 2005年 / 435卷
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摘要
Autoimmune reactions, in which the body's white blood cells harm its own tissues, cause many diseases including diabetes, multiple sclerosis and arthritis. It is not known why immune cells target certain organs, and in particular for childhood diabetes, why only insulin-producing cells are killed. Nakayama et al. now report that this may be because insulin itself is a primary autoantigen for autoimmune diabetes. In NOD mice, the standard animal model for diabetes, when the part of the insulin molecule that gives rise to autoantibodies is altered, autoimmune diabetes disappears. This also suggests that deletional immune therapy could be a practical proposition. The possible clinical relevance of this work is confirmed by a separate study by Kent et al. of human patients with type 1 diabetes. T lymphocytes found in the draining lymph nodes around the pancreas specifically recognize part of the insulin protein. This has implications for antigen specific therapies and islet-cell transplantation in diabetes.
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页码:220 / 223
页数:3
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