The first 2 authors contributed equally to this paper.
Expression and activity of IL-17 in cutaneous T-cell lymphomas (mycosis fungoides and sezary syndrome)
Version of Record online: 2 JUN 2004
Copyright © 2004 Wiley-Liss, Inc.
International Journal of Cancer
Volume 112, Issue 1, pages 113–120, 20 October 2004
How to Cite
Cirée, A., Michel, L., Camilleri-Bröet, S., Jean Louis, F., Oster, M., Flageul, B., Senet, P., Fossiez, F., Fridman, W. H., Bachelez, H. and Tartour, E. (2004), Expression and activity of IL-17 in cutaneous T-cell lymphomas (mycosis fungoides and sezary syndrome). Int. J. Cancer, 112: 113–120. doi: 10.1002/ijc.20373
- Issue online: 9 AUG 2004
- Version of Record online: 2 JUN 2004
- Manuscript Accepted: 18 MAR 2004
- Manuscript Received: 14 NOV 2003
- Fondation de France
- Association pour la Recherche sur le Cancer. Grant Number: 970RC24
- Ligue Nationale contre le Cancer
- Université René Descartes
- tumor microenvironment;
- polymorphonuclear neutrophil
Interleukin-17 (IL-17) is a proinflammatory cytokine mainly produced by activated CD4+ CD45RO T cells. In mice, we have demonstrated that, depending on the model, IL-17 may act as a tumor growth-promoting or -inhibiting factor. In order to address the relevance of these models in human tumors, we look for the natural expression and activity of IL-17 in mycosis fungoides (MF) and Sezary syndrome (SS). These cutaneous T-cell lymphomas were selected because they are usually CD3+ CD4+ CD45RO+, a phenotype similar to nontransformed T cells producing IL-17. We show that in vitro activated malignant T cells derived from MF or SS patients express IL-17 mRNA and secrete this cytokine. However, IL-17 does not act in vitro as a growth factor for MF or SS cell lines. In addition, 5 out of 10 MF/SS biopsies expressed IL-17 mRNA, while this cytokine was not detected in normal skin. IL-17 was not observed in the biopsies derived from 2 patients initially identified as MF, whereas an upregulation of this cytokine was clearly demonstrated during progression of the disease in these patients. An association between IL-17 expression and polymorphonuclear neutrophil infiltration was also recorded in this group of MF/SS patients. A more detailed analysis of 2 patients with a pustular form of MF and SS revealed that IL-17 may participate in the recruitment of polymorphonuclear neutrophils via a paracrine mechanism involving keratinocyte-released IL-8. This study is the first report demonstrating that some human tumor cells could express IL-17, a cytokine that represents an early event in the development of the inflammatory reaction within the tumor microenvironment, a process that may influence tumor phenotype and growth. © 2004 Wiley-Liss, Inc.