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The Journal of Immunology, 2003, 170: 749-756.
Copyright © 2003 by The American Association of Immunologists

Down-Modulation of Responses to Type I IFN Upon T Cell Activation1

Elisabetta Dondi*, Lars Rogge{dagger}, Georges Lutfalla{ddagger}, Gilles Uzé{ddagger} and Sandra Pellegrini2,*

* Unité de Signalisation des Cytokines and {dagger} Laboratoire de Immunorégulation, Institut Pasteur, Paris, France; and {ddagger} Centre National de la Recherche Scientifique Unité Mixte de Recherche 5124, Institut de Génétique Moléculaire, Montpellier, France

The immunomodulatory role of type I IFNs (IFN-{alpha}/{beta}) in shaping T cell responses has been demonstrated, but the direct effects of IFN on T cells are still poorly characterized. Particularly, because IFN exert an antiproliferative activity, it remains elusive how the clonal expansion of effector T cells can paradoxically occur in the event of an infection when large amounts of IFN are produced. To address this issue, we have studied the effects of type I IFN in an in vitro differentiation model of human primary CD4+ T cells. We found that IFN-{alpha} treatment of resting naive T cells delayed their entry into the cell cycle after TCR triggering. Conversely, the ongoing expansion of effector T cells was not inhibited by the presence of IFN. Moreover, activated T cells showed a significantly reduced induction of IFN-sensitive genes, as compared with naive precursors, and this decline occurred independently of subset-specific polarization. The residual type I IFN response measured in activated T cells was found sufficient to inhibit replication of the vesicular stomatitis virus. Our data suggest that the activation of T lymphocytes includes regulatory processes that restrain the transcriptional response to IFN and allow the proliferation of effector cells in the presence of this cytokine.


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