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[Cancer Research 59, 3698-3704, August 1, 1999]
© 1999 American Association for Cancer Research

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[Cancer Research 59, 3698-3704, August 1, 1999]
© 1999 American Association for Cancer Research


Immunology

Interleukin 17, a T-cell-derived Cytokine, Promotes Tumorigenicity of Human Cervical Tumors in Nude Mice1

Eric Tartour2, François Fossiez, Isabelle Joyeux, Annie Galinha, Alain Gey, Emmanuel Claret, Xavier Sastre-Garau, Jérôme Couturier, Veronique Mosseri, Virginie Vives, Jacques Banchereau, Wolf H. Fridman, John Wijdenes, Serge Lebecque and Catherine Sautèes-Fridman

Unité d’Immunologie Clinique, INSERM U 225 and Université Pierre et Marie Curie [E. T., I. J., A. Ga., A. Ge., V. V., W. H. F., C. S-F.], Département de Pathologie [X. S-G., J. C.], and Unité de Biostatistique [V. M.], Institut Curie, 75248 Paris, Cedex 05, France; Schering Plough, 69571 Dardilly, France [F. F., J. B., S. L.]; and Diaclone, BP1985, F25020 Besançon, France [E. C., J. W.]

Interleukin (IL) 17 is a proinflammatory cytokine secreted mainly by activated human memory CD4 T cells that induces IL-6, IL-8, and nitric oxide. Because IL-6 and IL-8 have been implicated in the pathogenesis of cervical cancer, we investigated the action of IL-17 on human cervical tumor cell lines in vitro and in vivo. We showed that in vitro, IL-17 increases IL-6 and IL-8 secretion by cervical carcinoma cell lines at both protein and mRNA levels. No direct effect of IL-17 on in vitro proliferation of cervical tumor cell lines could be demonstrated. However, two cervical cell lines transfected with a cDNA encoding IL-17 exhibited a significant increase in tumor size as compared to the parent tumor when transplanted in nude mice. This enhanced tumor growth elicited by IL-17 was associated with increased expression of IL-6 and macrophage recruitment at the tumor site. A potential role of IL-17 in modulation of the human cervical tumor phenotype was also supported by its expression on the cervical tumor in patients with CD4 infiltration. IL-17 therefore behaves like a T-cell-specific cytokine with paradoxical tumor-promoting activity. This may partially explain previous reports concerning the deleterious effect of CD4 T cells in cancer.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
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Copyright © 1999 by the American Association for Cancer Research.