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Ligand-Independent Down-Regulation of IFN- Receptor 1 Following TCR Engagement¹

Heidi Skrenta^2,*, Yang Yang, Sidney Pestka^* and C. Garrison Fathman^3,

^* Department of Molecular Genetics and Microbiology, Robert Wood Johnson Medical School-University of Medicine and Dentistry of New Jersey, Piscataway, NJ 08854; and Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305

Activated T lymphocytes modulate the level of many molecules on their cell surface, including cytokine receptors. This regulation of cytokine receptor expression affects the ability of T cells to respond to cytokines and thus influences the outcome of an immune response. The receptor for IFN-, a proinflammatory cytokine, consists of two copies of a ligand binding chain (IFN-R1) as well as two copies of a second chain (IFN-R2) required for signal transduction. The expression of IFN-R2 is down-regulated at the mRNA level on CD4⁺ T cells when they differentiate into the Th1, but not the Th2, phenotype. This down-regulation has been demonstrated to depend on the ligand, IFN-, which is produced by Th1 but not Th2 T cells. The regulation of the cell-surface expression of IFN- receptors during primary T cell activation has not been reported. Naive and differentiated T lymphocytes express IFN-R1 at the mRNA level and as a cell-surface protein. In this study, we present evidence that cell-surface expression of IFN-R1 is transiently down-regulated on the surface of naive CD4⁺ T cells shortly after TCR engagement. Furthermore, this down-regulation is not mediated by the ligand, IFN-, but results from TCR engagement and can be inhibited by cyclosporin A.

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