Cultured BALB/c islets fail to function when transplanted into diabetic nonobesediabetic (NOD) mice; such grafted tissue is rapidly destroyed by disease recurrence. The cellular requirements for this graft damage are unclear. This study was designed to investigate the role of the L3T4+ T-lymphocyte subset in disease recurrence in the NOD mouse. L3T4+ T-lymphocytes were depleted by the in vivo administration of the L3T4-specific monoclonal antibody GK1.5. This treatment reduced the level of L3T4+ T-lymphocytes from an initial 43% of the peripheral blood lymphocytes to 4%. L3T4 levels remained at this low level for ∼2 wk after withdrawal of GK1.5 treatment, after which the L3T4 levels slowly began to increase in the periphery. Grafting of cultured BALB/c islet tissue into GK 1.5-treated diabetic NOD mice resulted in a rapid return to normoglycemia that persisted for 2-4 wk. The gradual return to the hyperglycemic condition roughly correlated with the reappearance of L3T4+ T-lymphocytes in the peripheral circulation. From these findings we conclude that the disease process in the NOD mouse is L3T4 T-lymphocyte dependent.
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Rapid Publications| April 01 1987
Autoimmune Diabetes in NOD Mouse Is L3T4 T-Lymphocyte Dependent
Ronald G Gill;
Address correspondence and reprint requests to Dr. Kevin J. Lafferty, Dept. of Microbiology/Immunology, Barbara Davis Center, 4200 East 9th Avenue, Denver, CO 80262.
Yi Wang, Liming Hao, Ronald G Gill, Kevin J Lafferty; Autoimmune Diabetes in NOD Mouse Is L3T4 T-Lymphocyte Dependent. Diabetes 1 April 1987; 36 (4): 535–538. https://doi.org/10.2337/diab.36.4.535
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