ROLE OF LYMPHOKINE IN ISLET ALLOGRAFT REJECTION
- 1 March 1990
- journal article
- research article
- Published by Wolters Kluwer Health in Transplantation
- Vol. 49 (3), 609-614
- https://doi.org/10.1097/00007890-199003000-00025
Abstract
Primed CD8 T cells transfer allograft immunity to an established islet allograft. However, the process is inhibited by cyclosporine, suggesting that lymphokine production is required for islet graft rejection. The alloreactive T cell clone L3 will transfer allograft immunity, and this process is also sensitive to CsA. The L3 clone produces gamma-interferon and tumor necrosis factor but not IL-2 and IL-3. It follows therefore that the latter lymphokines are not required for the rejection process. Pretreatment of islet tissue with γ-IFN prior to grafting increases the density of the class I major histocompatibility complex antigen on the islet tissue, and CsA can no longer block the destruction of this MHC-induced tissue by primed alloreactive T cells. We conclude that γ-IFN, and possibly TNF, act cooperatively with cytotoxic function in the process of islet allograft rejection.This publication has 12 references indexed in Scilit:
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