Role of lymphokine in islet allograft rejection

Transplantation. 1990 Mar;49(3):609-14. doi: 10.1097/00007890-199003000-00025.


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 gamma-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 gamma-IFN, and possibly TNF, act cooperatively with cytotoxic function in the process of islet allograft rejection.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigens, Differentiation, T-Lymphocyte / analysis
  • CD4-Positive T-Lymphocytes / immunology
  • CD8 Antigens
  • Graft Rejection*
  • H-2 Antigens / immunology
  • Interferon-gamma / physiology
  • Interleukin-2 / physiology
  • Interleukin-3 / physiology
  • Islets of Langerhans Transplantation*
  • Lymphocyte Activation
  • Lymphokines / physiology*
  • Major Histocompatibility Complex
  • Mice
  • Mice, Inbred Strains
  • T-Lymphocytes / immunology*
  • Tumor Necrosis Factor-alpha / physiology


  • Antigens, Differentiation, T-Lymphocyte
  • CD8 Antigens
  • H-2 Antigens
  • Interleukin-2
  • Interleukin-3
  • Lymphokines
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma