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Cutting Edge: An Alternative Pathway of CD4⁺ T Cell Differentiation Is Induced Following Activation in the Absence of -Chain-Dependent Cytokine Signals¹

Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01655

This report addresses the role of -chain cytokine signals in regulating CD4⁺ T cell differentiation following activation. Using murine CD4⁺ T cells lacking the Jak3 tyrosine kinase, we show that activation of these cells in the absence of -chain-dependent cytokine signals induces an alternative pathway of T cell differentiation. Specifically, activated Jak3^–/– CD4⁺ T cells produce IL-10, TGF-, and IFN-, but not IL-2 or IL-4, and are unable to proliferate in vitro. In addition, Jak3^–/– CD4⁺ T cells express high levels of programmed death-1 and lymphocyte activation gene-3 and modestly suppress the proliferation of wild-type CD4⁺ T cells in coculture assays. Together, these features demonstrate a striking similarity between Jak3^–/– CD4⁺ T cells and the regulatory T cells that have been shown to suppress immune responses in vitro and in vivo. We conclude that Jak3 is a critical component of signaling pathways that regulate T cell differentiation into effector vs regulatory lineages.

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