Expanded T cells from pancreatic lymph nodes of type 1 diabetic subjects recognize an insulin epitope

Sally C. Kent, Yahua Chen, Lisa Bregoli, Sue M. Clemmings, Norma Sue Kenyon, Camillo Ricordi, Bernhard J. Hering and David A. Hafler ()
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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

Nature, 2005, vol. 435, issue 7039, 224-228

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/nature03625

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