Abstract
Clinical islet transplantation is now established as a treatment for patients with type I diabetes. Although organs from brain-dead (BD) donors are the main source for clinical transplantation, marginal status after BD produces deterioration of the organs followed by molecular activation. The effect of brain-death (BD) induction on the immunological status of donor islets was investigated using a rodent model of BD. BD animals showed decreased levels of peripheral white blood cells (WBC) compared to controls, indicating the extravasation of these cells (7270 ± 500 vs 9570 ± 370, respectively). In a densitometric study of RT-PCR products, the Th2 cytokine (IL-10) was significantly up-regulated in BD (2.91 ± 0.26 vs 1.76 ± 0.40), but a Th1 cytokine (IL-2) showed minimal change. Increased expression of IL-10 may inhibit macrophage function. As the marginal status after BD deteriorates, the islets of these donors may display early graft loss or poor long-term function. Integrative studies of immunomodulation might be necessary to eliminate islet infiltrates.
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