Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice
Maki Nakayama,
Norio Abiru,
Hiroaki Moriyama,
Naru Babaya,
Edwin Liu,
Dongmei Miao,
Liping Yu,
Dale R. Wegmann,
John C. Hutton,
John F. Elliott and
George S. Eisenbarth ()
Additional contact information
Maki Nakayama: University of Colorado Health Sciences Center
Norio Abiru: Nagasaki University
Hiroaki Moriyama: Kobe University Graduate School of Medicine
Naru Babaya: University of Colorado Health Sciences Center
Edwin Liu: University of Colorado Health Sciences Center
Dongmei Miao: University of Colorado Health Sciences Center
Liping Yu: University of Colorado Health Sciences Center
Dale R. Wegmann: University of Colorado Health Sciences Center
John C. Hutton: University of Colorado Health Sciences Center
John F. Elliott: University of Alberta
George S. Eisenbarth: University of Colorado Health Sciences Center
Nature, 2005, vol. 435, issue 7039, 220-223
Abstract:
Insulin sparks autoimmunity 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.
Date: 2005
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DOI: 10.1038/nature03523
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