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* Immunology Division, Department of Pediatrics, and
Pulmonary Division, Department of Medicine, Faculty of Medicine and Health Sciences, University of Sherbrooke, Québec, Canada; and
Centre de Recherche Clinique Etienne-Le Bel, Centre Hospitalier de l’Université de Sherbrooke, Sherbrooke, Québec, Canada
Recent reports have shown that IL-21, in synergy with IL-15, stimulates proliferation of CD8+ T lymphocytes in the absence of signaling via the TCR. In this study, we show that IL-6, which induces phosphorylation of STAT3 similarly to IL-21, also can stimulate proliferation of CD8+ T cells in synergy with IL-7 or IL-15. IL-6 displays a stronger synergy with IL-7 than with IL-15 to stimulate naive CD8+ T cells. Concomitant stimulation by IL-6 or IL-21 augments phosphorylation and DNA-binding activity of STAT5 induced by IL-7 or IL-15. Like IL-21, IL-6 reduces the TCR signaling threshold required to stimulate CD8+ T cells. Prior culture of P14 TCR transgenic CD8 T cells with IL-6 or IL-21 in the presence of IL-7 or IL-15 augments their proliferation and cytolytic activity upon subsequent stimulation by Ag. Furthermore, cytokine stimulation induces quantitatively and qualitatively distinct phenotypic changes on CD8+ T cells compared with those induced by TCR signaling. We propose that the ability of IL-6 to induce TCR-independent activation of CD8+ T cells in synergy with IL-7 or IL-15 may play an important role in the transition from innate to adaptive immunity.
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1 This work was supported by a Canadian Institutes of Health Research grant to S.I. (MOP-62800) and by the Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, and Centre de Recherche Clinique Étienne-Le Bel du Centre Hospitalier Universitaire de Sherbrooke. S.I. was a scholar of the Fonds de la Recherche en Santé du Québec and is a Canadian Institutes of Health Research new investigator. P.P.M. is a Fonds de la Recherche en Santé du Québec scholar. J.G. is supported by a Fonds de la Recherche en Santé du Québec doctoral studentship. A.C. is a recipient of Canadian Institutes of Health Research doctoral studentship.
2 J.G. and S.R. contributed equally to this work.
3 Address correspondence and reprint requests to Dr. Subburaj Ilangumaran, Immunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, 3001 North 12th Avenue, Sherbrooke, Québec J1H 5N4, Canada. E-mail address: Subburaj.Ilangumaran{at}Usherbrooke.ca
4 Abbreviations used in this paper: 
c, common -chain; GRR, IFN- response region; PTK, protein tyrosine kinase; tg, transgenic.
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