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Immune mechanisms that regulate susceptibility to autoimmune type I diabetes

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Conclusion

Type I diabetes is an autoimmune disease heralded by T cell-mediated destruction of pancreatic islet β cells. The mechanism(s) involved in this β-cell destruction is not precisely understood. There is evidence that the etiology of disease is owing to a complex interaction between genes and the environment and that the pathogenesis is autoimmune in nature. With the availability of major new tools such as β cell-specific autoantigens, gene knockout and transgenic mice, and various cytokines, the mechanism of disease induction, progression, and regulation will be elucidated in the near future. A better understanding of the pathogenesis of type I diabetes may provide novel therapeutic agents for the prevention of the disease.

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Authors and Affiliations

  1. Department of Microbiology, University of Western Ontario, N6A 5C1, London, Ontario, Canada

    Bhagirath Singh

  2. Department of Immunology, University of Western Ontario, N6A 5C1, London, Ontario, Canada

    Bhagirath Singh

  3. Autoimmunity/Diabetes Group, The John P. Robarts Research Institute, 1400 Western Road, N6G 2V4, London, Ontario, Canada

    Terry L. Delovitch

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  1. Bhagirath Singh
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  2. Terry L. Delovitch
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Correspondence to Terry L. Delovitch.

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Singh, B., Delovitch, T.L. Immune mechanisms that regulate susceptibility to autoimmune type I diabetes. Clinic Rev Allerg Immunol 19, 247–264 (2000). https://doi.org/10.1385/CRIAI:19:3:247

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