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Updated: Jul 5, 2026

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
[Interleukin-1 and nitric oxide involved in the pathogenesis of diabetes)]
1Rolf Lufts centrum för diabetesforskning, Karolinska sjukhuset, Stockholm. ake@enk.ks.se
Abstract:
Insulin-dependent diabetes mellitus (IDDM) is not only a common metabolic disorder in industrialised countries, but its incidence is still increasing, especially in Scandinavia. The article consists in a review of evidence implicating nitric oxide (NO) and the cytokine, interleukin-1 (IL-1), in the pathogenesis of IDDM. Cytotoxic effects of IL-1 and NO, generated through autoimmune reactions associated with insulitis and impairing the function of insulin-producing pancreatic beta-cells in IDDM, are discussed, as are possible pharmacological strategies for blocking this toxicity. Compounds capable of blocking IL-1 cell surface receptors and NO synthesis may prove beneficial in protecting beta-cells from autoimmune assault in IDDM. If IL-1 causes beta-cell dysfunction and destruction through NO synthesis in IDDM, several pathways in the IL-1-NO system are attractive potential targets for drugs protecting beta-cells against these effects, thus providing a means of intervening in the pathogenesis of IDDM.
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