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Critical Reviews™ in Immunology
Fator do impacto: 1.404 FI de cinco anos: 3.347 SJR: 0.706 SNIP: 0.55 CiteScore™: 2.19

ISSN Imprimir: 1040-8401
ISSN On-line: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v22.i4.50
33 pages

Role of IFN-g in Allograft Rejection

Luis G. Hidalgo
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada
Philip F. Halloran
Departments of Medical Microbiology and Immunology, and Department of Medicine, University of Alberta, Edmonton, Alberta, Canada


Interferon (IFN)-g is a cytokine produced mostly by activated T cells and NK cells that has complex effects on immune and nonimmune cells. IFN-g plays important roles in inflammation, usually in synergy with other cytokines, such as IL-1b and TNF-a. The uniqueness of IFN-g lies in its ability to induce major histocompatibility complex (MHC) expression in many tissues, making it particularly relevant to transplantation. The results of graft rejection in the absence of IFN-g show that IFN-g modulates but is not essential for the allogeneic responses, suppressing generation of CTL. In vivo IFN-g has a protective role early in the response to vascularized organ allografts: transplants in mice have a tendency to develop necrosis when IFN-g is not available, apparently by failure of the microcirculation. The lack of IFN-g greatly reduces the induction of MHC in organ allografts, and it is possible that this is indirectly related to the protective effect of IFN-g. Nevertheless IFN-g also promotes graft vessel disease later in the course of the transplant. Thus IFN-g has diverse and potentially contradictory effects on organ allograft survival, acting both on the immune system and on the graft itself, the net effect depending on the graft type and the time post-transplant.

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