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¹ Department of Internal Medicine and DENOTHE Center, ² Department of Gynecology, Perinatology and Human Reproduction, and ³ Department of Pathophysiology, University of Florence, Florence 50134, Italy
⁴ Department of Clinical and Experimental Medicine, Second University of Naples and Centro Regionale di Competenza in Genomica, Naples 80131, Italy
⁵ Section of Pharmacological Sciences, Second University of Naples, Naples 80131, Italy
⁶ Department of Dermatological Sciences, University of Florence, Florence 50121, Italy

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

We demonstrate that CD161 is a highly up-regulated gene in human interleukin (IL) 17 T helper cell (Th17) clones and that all IL-17–producing cells are contained in the CD161⁺ fraction of CD4⁺ T cells present in the circulation or in inflamed tissues, although they are not CD1-restricted natural killer T cells. More importantly, we show that all IL-17–producing cells originate from CD161⁺ naive CD4⁺ T cells of umbilical cord blood, as well as of the postnatal thymus, in response to the combined activity of IL-1β and IL-23. These findings implicate CD161 as a novel surface marker for human Th17 cells and demonstrate the exclusive origin of these cells from a CD161⁺CD4⁺ T cell progenitor.

Abbreviations used: APC, allophycocyanin; CD, Crohn's disease; CLEC2, C-type lectin domain family 2; iNKT, invariant NKT; MNC, mononuclear cell; NKT, natural killer T; PB, peripheral blood; PPD, purified protein derivative; RORt, retinoic acid–related orphan receptor t; TREC, TCR excision circle; UCB, umbilical cord blood.

L. Cosmi and R. De Palma contributed equally to this paper.

© 2008 Cosmi et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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