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Roles of cytokines in the pathogenesis and therapy of type 1 diabetes

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Abstract

Type 1 diabetes (T1D) results from autoimmune destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans by autoreactive T helper 1 (Th1) cells characterized by their cytokine secretory products, interleukin-2 (IL-2) and interferon γ (IFNγ). Th1-type cytokines (IL-2 and IFNγ) correlate with T1D, whereas Th2 (IL-4 and IL-10), Th3 (transforming growth factor beta [TGFβ]), and T regulatory cell-type cytokines (IL-10 and TGFβ) correlate with protection from T1D. Paradoxically, however, administrations of Th1-type cytokines (IL-2 and IFNγ) and immunotherapies that induce Th1-type cytokine responses actually prevent T1D, at least in animal models. Therefore, immunotherapies that inhibit IL-2 production/action will block Th1 cell/cytokine-driven effector mechanisms of pancreatic islet β-cell destruction; however, anti-IL-2 therapy will not allow immune tolerance to be established. In contrast, immunotherapies that increase IL-2 production/action may correct an immunodeficiency in IL-2 production that appears to underlie the autoimmunity of T1D, thereby restoring immune tolerance to islet β-cells and prevention of T1D.

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  1. Department of Medicine, University of Alberta, Edmonton, AB, Canada

    Alex Rabinovitch & Wilma L. Suarez-Pinzon

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  1. Alex Rabinovitch
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  2. Wilma L. Suarez-Pinzon
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Correspondence to Alex Rabinovitch.

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Rabinovitch, A., Suarez-Pinzon, W.L. Roles of cytokines in the pathogenesis and therapy of type 1 diabetes. Cell Biochem Biophys 48, 159–163 (2007). https://doi.org/10.1007/s12013-007-0029-2

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  • DOI: https://doi.org/10.1007/s12013-007-0029-2

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