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  • Title: IFN-gamma is critical for long-term allograft survival induced by blocking the CD28 and CD40 ligand T cell costimulation pathways.
    Author: Konieczny BT, Dai Z, Elwood ET, Saleem S, Linsley PS, Baddoura FK, Larsen CP, Pearson TC, Lakkis FG.
    Journal: J Immunol; 1998 Mar 01; 160(5):2059-64. PubMed ID: 9498741.
    Abstract:
    It is postulated that IFN-gamma production hinders long-term acceptance of transplanted organs. To test this hypothesis, we compared survival of skin and heart allografts in wild-type (IFN-gamma+/+) mice to that in IFN-gamma gene knockout (IFN-gamma-/-) mice. We found that perioperative blockade of the CD28 and/or CD40 ligand T cell costimulation pathways induces long-term skin and heart allograft survival in IFN-gamma+/+ recipients but fails to do so in IFN-gamma-/- mice or in wild-type mice treated with IFN-gamma-neutralizing Ab at the time of transplantation. In vitro studies showed that endogenously produced IFN-gamma down-regulates T cell proliferation and CTL generation in MLCs. These actions of IFN-gamma were not mediated by TNF-alpha production or Fas-Fas ligand interactions. In vivo studies revealed exaggerated expansion and, subsequently, impaired deletion of superantigen-reactive T lymphocytes in IFN-gamma-/- mice injected with staphylococcal enterotoxin B. Taken together, our findings indicate that IFN-gamma does not hinder but instead facilitates induction of long-term allograft survival possibly by limiting expansion of activated T cells.
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