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 Blood, 22 October 2009, Vol. 114, No. 17, pp. 3610-3614.
Prepublished online as a Blood First Edition Paper on August 24, 2009; DOI 10.1182/blood-2009-05-223768.

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IMMUNOBIOLOGY

Brief report

Multiparametric analysis of cytokine-driven human Th17 differentiation reveals a differential regulation of IL-17 and IL-22 production

Elisabetta Volpe1,2, Maxime Touzot1,3, Nicolas Servant46, Marie-Annick Marloie-Provost1,3, Philippe Hupé47, Emmanuel Barillot46, and Vassili Soumelis1,3

1 Institut Curie, Laboratoire d'Immunologie Clinique, Paris, France; and 2 Fondazione Santa Lucia, Laboratorio Neuroimmunologia, Rome, Italy; 3 Inserm U932, Paris, France; 4 Institut Curie, Bioinformatique et Biologie des Systèmes, Paris, France; 5 Inserm U900, Paris, France; 6 Ecole des Mines de Paris, ParisTech, Fontainebleau, France; and 7 Centre National de la Recherche Scientifique, Unite Mixte de Recherche 144, Paris, France

T helper 17 (Th17) cells produce IL-17 but can also make tumor necrosis factor, interleukin (IL)–6, IL-10, IL-21, and IL-22. These cytokines collectively contribute to the functional outcome of the Th response. IL-22 plays a critical role in some Th17-associated diseases, such as psoriasis, but its relationship to IL-17 remains controversial. Here, we used a systematic multiparametric analysis of Th-17-associated cytokines, which revealed the unexpected finding that the regulation pattern of IL-22 was most closely related to interferon-{gamma}, the prototypical Th1 cytokine, and not to IL-17. To explain this observation, we systematically tested the role of Th1- and Th17-inducing cytokines. We could show that IL-12 and IL-23 induced high levels of IL-22 but no IL-17. Conversely, transforming growth factor-β inhibited IL-22 production but promoted IL-17. Thus, IL-17 and IL-22 are differentially regulated during cytokine-induced Th cell differentiation. This has important implications for the understanding and pharmacologic manipulation of Th17-associated pathologies.


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