In autoimmune (type 1) diabetes T-cells recognize pancreatic antigens and initiate a leukocyte infiltrate that produces proinflammatory cytokines and reactive oxygen species, ultimately leading to ß-cell destruction. In February Diabetes, Jon Piganelli and colleagues from University of Colorado Health Sciences Center, Denver, Colorado, show that the antioxidant metalloporphyrin-based superoxide dismutase (SOD) can prevent or delay the onset of the autoimmune cascade in diabetes.

Piganelli et al. used a diabetogenic T-cell clone to induce rapid onset of diabetes in young nonobese diabetic-severe combined immunodeficient (NOD.scid) mice. In these animals they found that diabetes was significantly delayed or even prevented if mice were pre-treated with an SOD mimic, AEOL-10113. In vitro, SOD significantly inhibited antigen-presenting cell-dependent T-cell proliferation and IFN-γ production. In addition, SOD inhibited the LPS-dependent increase in TNF-α as well as the NADPH oxidase-dependent release of superoxide (Diabetes 2002, 51:347-355).

"These data...

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