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Diabetes 51:347-355, 2002
© 2002 by the American Diabetes Association, Inc.

A Metalloporphyrin-Based Superoxide Dismutase Mimic Inhibits Adoptive Transfer of Autoimmune Diabetes by a Diabetogenic T-Cell Clone

Jon D. Piganelli1, Sonia C. Flores2, Coral Cruz2, Jeffrey Koepp2, Ines Batinic-Haberle3, James Crapo4, Brian Day4, Remy Kachadourian4, Rebekah Young1, Brenda Bradley1, and Kathryn Haskins1

1 Department of Immunology, University of Colorado Health Sciences Center and Barbara Davis Center for Childhood Diabetes, Denver, Colorado
2 Webb-Waring Institute for Antioxidant Research, Denver, Colorado
3 Department of Biochemistry, Duke University Medical Center, Durham, North Carolina
4 National Jewish Medical and Research Center, Denver, Colorado

We present here the first report of a metalloporphyrin-based antioxidant that can prevent or delay the onset of autoimmune diabetes. Type 1 diabetes is an autoimmune process whereby T-cells recognize pancreatic ß-cell antigens and initiate a leukocyte infiltrate that produces proinflammatory cytokines and reactive oxygen species (ROS), ultimately leading to ß-cell destruction. Because islet ß-cells have a reduced capacity to scavenge free radicals, they are very sensitive to ROS action. Metalloporphyrin-based superoxide dismutase (SOD) mimics scavenge ROS and protect cells from oxidative stress and apoptosis. To investigate the effect of SOD mimics and the role of oxidative stress in the development of autoimmune diabetes in vivo, we used a diabetogenic T-cell clone, BDC-2.5, to induce rapid onset of diabetes in young nonobese diabetic-severe combined immunodeficient mice (NOD.scid). Disease was significantly delayed or prevented altogether by treatment of recipient mice with an SOD mimic, AEOL-10113, before transfer of the BDC-2.5 clone. To investigate the mechanisms of protection, in vitro assays for T-cell proliferation and {gamma}-interferon (IFN-{gamma}) production were carried out using the T-cell clone BDC-2.5. We found that the SOD mimic significantly inhibited antigen-presenting cell-dependent T-cell proliferation and IFN-{gamma} production in vitro. In addition, pretreatment of lipopolysaccharide (LPS)-stimulated peritoneal macrophages with SOD mimic inhibited the LPS-dependent increase in TNF-{alpha} as well as the NADPH oxidase-dependent release of superoxide. Finally, this compound protected NIT-1 insulinoma cells from interleukin-1ß and alloxan cytotoxicity in vitro.


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