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

Author

Listed:
  • 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)

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

  • 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, 2005. "Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice," Nature, Nature, vol. 435(7039), pages 220-223, May.
  • Handle: RePEc:nat:nature:v:435:y:2005:i:7039:d:10.1038_nature03523
    DOI: 10.1038/nature03523
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    Cited by:

    1. Hao Hu & Anthony N. Vomund & Orion J. Peterson & Neetu Srivastava & Tiandao Li & Lisa Kain & Wandy L. Beatty & Bo Zhang & Chyi-Song Hsieh & Luc Teyton & Cheryl F. Lichti & Emil R. Unanue & Xiaoxiao Wa, 2024. "Crinophagic granules in pancreatic β cells contribute to mouse autoimmune diabetes by diversifying pathogenic epitope repertoire," Nature Communications, Nature, vol. 15(1), pages 1-22, December.

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