ABSTRACT
Most patients who develop insulin dependent diabetes mellitus suffer immu-nologically sustained loss of pancreatic beta islet cell function. Inheritance of genes positioned within the major histocompatibility complex render certain individuals susceptible to this autoimmune state. While corticosteroids block T cell proliferation, it is ironic that the primary target of corticosteroids may not actually be the T cell. Corticosteroids block T cell proliferation through their ability to block activation of accessory cells. Cyclosporine blocks the T cell activation cascade at a slightly more distal step than corticosteroids. New high tech approaches have great promise for refining the focus of immunosuppressive protocols. The presence of IL-2R on all recently activated T cells, and their absence from the surface of almost all resting or memory T cells, makes it possible to target only the relevant responding clones following an allograft, raising the hope of highly selective immunosuppression.
