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The Journal of Immunology, 2004, 173: 3740-3747.
Copyright © 2004 by The American Association of Immunologists

A Dual Role of IFN-{alpha} in the Balance between Proliferation and Death of Human CD4+ T Lymphocytes during Primary Response1

Elisabetta Dondi2,*, Gaël Roué{dagger}, Victor J. Yuste{dagger}, Santos A. Susin3,{dagger} and Sandra Pellegrini3,4,*

* Unité de Signalisation des Cytokines, and {dagger} Apoptose et Système Immunitaire, Institut Pasteur, Paris, France

Type I IFNs (IFN-{alpha}{beta}) enhance immune responses, notably T cell-mediated responses, in part by promoting the functional activities of dendritic cells. In this study, we analyzed the direct impact of IFN-{alpha} on proliferative and apoptotic signals upon in vitro activation of human naive CD4+ T lymphocytes. We demonstrate that IFN-{alpha} protects T cells from the intrinsic mitochondrial-dependent apoptosis early upon TCR/CD28 activation. IFN-{alpha} acts by delaying entry of cells into the G1 phase of the cell cycle, as well as by increasing Bcl-2 and limiting Bax activation. Later, upon activation, T cells that were exposed to IFN-{alpha} showed increased levels of surface Fas associated with partially processed caspase-8, a key component of the extrinsic apoptotic pathway. Caspase-8 processing was augmented furthermore by Fas ligation. Overall, these findings support a model whereby IFN-{alpha} favors an enhanced clonal expansion, yet it sensitizes cells to the Ag-induced cell death occurring at the end of an immune response. These observations point to a complex role of type I IFN in regulating the magnitude of proliferation and survival of naive CD4+ T cells during primary response and underline how crucial could be the timing of exposure to this cytokine.




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