The Journal of Experimental Medicine
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Published online July 16, 2007
doi:10.1084/jem.20070663
The Journal of Experimental Medicine, Vol. 204, No. 8, 1849-1861
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Annunziato et al.
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ARTICLE

 Phenotypic and functional features of human Th17 cells

Francesco Annunziato1, Lorenzo Cosmi1, Veronica Santarlasci1, Laura Maggi1, Francesco Liotta1, Benedetta Mazzinghi1, Eliana Parente1, Lucia Filì1, Simona Ferri1, Francesca Frosali1, Francesco Giudici2, Paola Romagnani1, Paola Parronchi1, Francesco Tonelli2, Enrico Maggi1, and Sergio Romagnani1

1 Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders (DENOTHE) and 2 Department of Pathophysiology, University of Florence, Florence 50134, Italy

CORRESPONDENCE Sergio Romagnani:s.romagnani{at}dmi.unifi.it

T helper (Th) 17 cells represent a novel subset of CD4+ T cells that are protective against extracellular microbes, but are responsible for autoimmune disorders in mice. However, their properties in humans are only partially known. We demonstrate the presence of Th17 cells, some of which produce both interleukin (IL)-17 and interferon (IFN)-{gamma} (Th17/Th1), in the gut of patients with Crohn's disease. Both Th17 and Th17/Th1 clones showed selective expression of IL-23R, CCR6, and the transcription factor ROR{gamma}t, and they exhibited similar functional features, such as the ability to help B cells, low cytotoxicity, and poor susceptibility to regulation by autologous regulatory T cells. Interestingly, these subsets also expressed the Th1-transcription factor T-bet, and stimulation of these cells in the presence of IL-12 down-regulated the expression of ROR{gamma}t and the production of IL-17, but induced IFN-{gamma}. These effects were partially inhibited in presence of IL-23. Similar receptor expression and functional capabilities were observed in freshly derived IL-17–producing peripheral blood and tonsillar CD4+ T cells. The demonstration of selective markers for human Th17 cells may help us to understand their pathogenic role. Moreover, the identification of a subset of cells sharing features of both Th1 and Th17, which can arise from the modulation of Th17 cells by IL-12, may raise new issues concerning developmental and/or functional relationships between Th17 and Th1.

Abbreviations used: Ab, antibody; CD, Crohn's disease; CIA, collagen-induced arthritis; EAE, experimental autoimmune encephalomyelitis; PB, peripheral blood; RA, rheumatoid arthritis.

F. Annunziato and L. Cosmi contributed equally to this paper.


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