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Regulation of IFN- Signaling Is Essential for the Cytotoxic Activity of CD8⁺ T Cells¹

Gregory Z. Tau^*, Simone N. Cowan, Jeffrey Weisburg, Ned S. Braunstein and Paul B. Rothman^2,,

^* Integrated Program in Cell, Molecular, and Biophysical Studies, Department of Medicine, and Department of Microbiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032

Previous studies have demonstrated that, as naive murine CD4⁺ cells differentiate into Th1 cells, they lose expression of the second chain of IFN-R (IFN-R2). Hence, the IFN--producing subset of Th cells is unresponsive to IFN-. Analysis of IFN--producing CD8⁺ T cells demonstrates that, like Th1 cells, these cells do not express IFN-R2. To define the importance of IFN- signaling for the development of functional CD8⁺ T cells, mice either lacking IFN-R2 or overexpressing this protein were examined. While CD8⁺ T cell development and function appear normal in IFN-R2^-/- mice, CD8⁺ T cell function in IFN-R2 transgenic is altered. IFN-R2 transgenic CD8⁺ T cells are unable to lyse target cells in vitro. However, these cells produce Fas ligand, perforin, and granzyme B, the effector molecules required for killing. Interestingly, TG CD8⁺ T cells proliferate normally and produce cytokines, such as IFN- in response to antigenic stimulation. Therefore, although IFN- signaling is not required for the generation of normal cytotoxic T cells, constitutive IFN- signaling can selectively impair the cytotoxic function of CD8⁺ T cells.

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