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*Institute for Neuroimmunology and Clinical Multiple Sclerosis Research, Center for Molecular Neurobiology Hamburg and
Department of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany;
Graduate School of Cellular and Molecular Neuroscience, University of Tübingen, Germany;
Interdisciplinary Clinic for Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany;
¶Division of Infection Immunology, Research Center Borstel, Borstel, Germany; and
||Cluster of Excellence Inflammation at Interfaces, Borstel-Kiel-Lübeck-Plön, Germany
Th17 cells are involved in the defense against bacteria and fungi and play a prominent role in the pathogenesis of autoimmune diseases, but research on human Th17 cells is hindered due to the lack of a surface marker. In this study, we report that a subset of human and mouse CD4+ T cells as well as human Th17 T cell clones express IL-17A on their surface upon stimulation. Correlation of surface IL-17A expression with intracellular IL-17A production and with ROR
t mRNA expression identified surface IL-17A as a specific marker for human and mouse Th17 cells. Phenotype characterization of ex vivo CD4+ IL-17A+ cells showed that the chemokines CCR6 and CCR4, costimulatory molecules, as well as CD2 and CD49d were more prominently expressed on these cells than in surface IL-17A– cells, supporting the concept of Th17 cells as a potent inflammatory effector subtype. In addition, we generated human Th1, Th1/17 (producing both IFN- and IL-17A), and Th17 T cell clones based on single cell sorting of surface IL-17A–, IL-17Aint, and IL-17Ahigh CD4+ T cells, respectively, and showed the plasticity of the double producing clones to the cytokine milieu. The identification of surface IL-17A as a marker for Th17 cells should facilitate research on this subset.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 The Institute for Neuroimmunology and Clinical Multiple Sclerosis Research and this work are supported by the Hertie Foundation. V.B.-W. was partly supported by the German Research Council (SFB 685) and C.H. by the Research Focus Autoimmunity at the University of Lübeck.
2 Address correspondence and reprint requests to Eva Tolosa, Department of Immunology, University Medical Center Hamburg-Eppendorf (UKE), Martinistr. 52, 20251 Hamburg, Germany. E-mail address: etolosa{at}uke.uni-hamburg.de
3 Abbreviations used in this paper: TCC, T cell clone; MFI, mean fluorescence intensity; ICS, intracellular cytokine staining; PD-1, programmed cell death 1; TMHMM, transmembrane prediction using hidden Markov models; MINNOU, membrane protein identification without explicit use of hydropathy profiles and alignments.
4 The online version of this article contains supplementary material.
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