Author
Listed:
- Sally C. Kent
(Brigham and Women's Hospital and Harvard Medical School)
- Yahua Chen
(Brigham and Women's Hospital and Harvard Medical School)
- Lisa Bregoli
(Brigham and Women's Hospital and Harvard Medical School)
- Sue M. Clemmings
(University of Minnesota)
- Norma Sue Kenyon
(University of Miami)
- Camillo Ricordi
(University of Miami)
- Bernhard J. Hering
(University of Minnesota)
- David A. Hafler
(Brigham and Women's Hospital and Harvard Medical School)
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.
Suggested Citation
Sally C. Kent & Yahua Chen & Lisa Bregoli & Sue M. Clemmings & Norma Sue Kenyon & Camillo Ricordi & Bernhard J. Hering & David A. Hafler, 2005.
"Expanded T cells from pancreatic lymph nodes of type 1 diabetic subjects recognize an insulin epitope,"
Nature, Nature, vol. 435(7039), pages 224-228, May.
Handle:
RePEc:nat:nature:v:435:y:2005:i:7039:d:10.1038_nature03625
DOI: 10.1038/nature03625
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