Interleukin-2-diphtheria toxin fusion protein prolongs murine islet cell engraftment

Transplantation
O PankewyczV E Kelley

Abstract

Allograft rejection is dependent upon complex cell-mediated processes, the primary effectors of which are activated T cells. As the expression of the cell surface protein interleukin 2 receptor is primarily limited to the subset of stimulated T cells, therapeutic agents that target this molecule may provide highly selective immunosuppression. A newly constructed chimeric IL-2 diphtheria toxin fusion protein specifically binds to and poisons activated T cells bearing the high-affinity IL-2R. We describe the in vivo effects of IL-2 toxin in preventing rejection of a crude pancreatic islet preparation transplanted across major and minor histoincompatibility barriers. IL-2 toxin administered once daily as the sole immunosuppressive agent prolongs islet graft survival and decreases the severity of the early mononuclear cell infiltrate into the graft site. Long-term survival of transplanted islets (greater than 100 days) was achieved following a short course (10 days) of more-intensive IL-2 toxin treatment. Thus IL-2 toxin, a highly selective immunosuppressive agent, leads to prolonged islet cell engraftment while sparing the resting or memory subset of the entire T cell repertoire.

Citations

Jan 1, 1991·Toxicon : Official Journal of the International Society on Toxinology·C R Carlini, J A Guimarães
Apr 1, 1989·Current Opinion in Immunology·O PankewyczV E Kelley
Jun 6, 2000·Advanced Drug Delivery Reviews·I Pastan, R J Kreitman
Apr 1, 1989·Kidney International·T B Strom, V E Kelley

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