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The Journal of Immunology, 2001, 167: 6637-6643.
Copyright © 2001 by The American Association of Immunologists

IFN-{gamma} Affects Homing of Diabetogenic T Cells1

Alexei Y. Savinov*, F. Susan Wong{dagger} and Alexander V. Chervonsky2,*

* The Jackson Laboratory, Bar Harbor, ME 04609; and {dagger} Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, Bristol, United Kingdom

IFN-{gamma} is a cytokine with pleiotropic functions that participates in immune and autoimmune responses. The lack of IFN-{gamma} is known to delay the development of autoimmune diabetes in nonobese diabetic (NOD) mice. Splenocytes from diabetic NOD and IFN-{gamma} knockout (KO) NOD mice transfer diabetes into NOD recipients equally well. However, adoptive transfer of diabetogenic T cells from NOD mice into NOD.IFN-{gamma}-KO or NOD mice lacking {beta}-chain of IFN-{gamma} receptor (NOD.IFN-{gamma}R{beta}-KO) appeared to be much less efficient. We found that IFN-{gamma} influences the ability of diabetogenic cells to penetrate pancreatic islets. Tracing in vivo of insulin-specific CD8+ T cells has shown that homing of these cells to the islets of Langerhans was affected by the lack of IFN-{gamma}. While adhesion of insulin-specific CD8+ cells to microvasculature was normal, the diapedesis was significantly impaired. This effect was reversible by treatment of the animals with rIFN-{gamma}. Thus, IFN-{gamma} may, among other effects, influence immune and autoimmune responses by supporting the homing of activated T cells.




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