Low-dose streptozotocin-induced diabetes in mice serves as a model of type Idiabetes. Suppression of the development of diabetes (hyperglycemia) in C3H/ He mice was achieved with in vivo administration of antibody reactive to Ir-gene products before streptozo-tocin treatment. A persistent effect was reached with two monoclonal antibodies directed against l-Ak gene products and, surprisingly, by an allo-antiserum to I-J determinants. These results suggest a role for I-A and I-J positive T-lymphocytes and/or macrophages in B-islet cell autoimmunity.

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