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The Journal of Immunology, 2000, 165: 247-255.
Copyright © 2000 by The American Association of Immunologists

An Essential Contribution by IFN-{gamma} to CD8+ T Cell-Mediated Rejection of Pancreatic Islet Allografts1

Andrew S. Diamond* and Ronald G. Gill2,{dagger}

Departments of * Immunology and {dagger} Medicine, Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver, CO 80262

CD8+ T cells have long been considered to be the prototypical cytotoxic lymphocyte subpopulation. However, whether alloreactive CD8+ T cells require traditional cytolytic pathways such as perforin and Fas ligand (FasL) to mediate graft rejection has been a controversial issue. In the present studies, we examined the role of varied effector pathways in CD8+ T cell-mediated rejection of pancreatic islet allografts. Our goal was to systematically determine the relative requirements, if any, of perforin and FasL as well as the proinflammatory cytokine IFN-{gamma} in triggering graft destruction. To study CD8+ T cell effector pathways independently of other lymphocyte populations, purified alloreactive CD8+ T cells were adoptively transferred into severe combined immune-deficient (SCID) recipients bearing established islet allografts. Results indicate that to reject established islet allografts, primed CD8+ T cells do not require the individual action of the conventional cytotoxic effectors perforin and Fas ligand. In contrast, the ability to produce IFN-{gamma} is critical for efficient CD8+ T cell-mediated rejection of established islet allografts. Furthermore, alloreactive CD8+ TCR transgenic T cells (2C) also show IFN-{gamma} dependence for mediating islet allograft rejection in vivo. We speculate from these results that the production of IFN-{gamma} by alloreactive CD8+ T cells is a rate-limiting step in the process of islet allograft rejection.




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