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Diabetes Publish Ahead of Print published online ahead of print April 24, 2007
DOI: 10.2337/db06-1632
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Original Research

Inhibition of autoimmune diabetes by oral administration of anti-CD3 monoclonal antibody

Hiroki Ishikawa1, Hirofumi Ochi1, Mei-Ling Chen1, Dan Frenkel1, Ruth Maron1, and Howard L. Weiner1

1Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston MA

Anti-CD3 monoclonal antibody has been shown to induce tolerance and be an effective treatment for diabetes both in animal models and in human trials. We have shown that anti-CD3 monoclonal antibody given orally is biologically active in the gut and suppresses experimental autoimmune encephalitis by the induction of a regulatory T cell that expresses latency associated peptide (LAP) on its surface. In the present study we investigated the effect of oral anti-CD3 on the prevention of autoimmune diabetes in AKR mice in which low dose streptozocin (STZ) model induces autoimmunity to the beta cells of the islets. We found that oral anti-CD3 given at doses of 50 and 250 µg/feeding suppressed the incidence of diabetes in this model with best effects seen at the 50 µg/dose . Associated with suppression we observed decreased cell proliferation in the spleen and conversion of Th1 responses into Th2/Th3 responses in the periphery including in the pancreatic lymph nodes. Oral anti-CD3 increased the expression of LAP on CD4+ T cells and these cells could adoptively transfer protection. Protection by oral anti-CD3 was TGF-ß dependent. Our results demonstrate that oral anti-CD3 is effective in the model of streptozocin diabetes and may be a useful form of therapy for type 1 diabetes in humans.


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Copyright © 2007 by the American Diabetes Association.