Journal article
CD3(bright) signals on gamma delta T cells identify IL-17A-producing V gamma 6V delta 1( ) T cells
C Paget, MT Chow, NA Gherardin, PA Beavis, AP Uldrich, H Duret, M Hassane, F Souza-Fonseca-Guimaraes, DA Mogilenko, D Staumont-Salle, NK Escalante, GR Hill, P Neeson, DS Ritchie, D Dombrowicz, T Mallevaey, F Trottein, GT Belz, DI Godfrey, MJ Smyth
IMMUNOLOGY AND CELL BIOLOGY | NATURE PUBLISHING GROUP | Published : 2015
DOI: 10.1038/icb.2014.94
Abstract
Interleukin-17A (IL-17A) is a pro-inflammatory cytokine that has an important role at mucosal sites in a wide range of immune responses including infection, allergy and auto-immunity. γδ T cells are recognized as IL-17 producers, but based on the level of CD3 expression, we now define the remarkable ability of a CD3(bright) γδ T-cell subset with an effector memory phenotype to rapidly produce IL-17A, but not interferon-γ. CD3(bright) γδ T cells uniformly express the canonical germline encoded Vγ6/Vδ1(+) T-cell receptor. They are widely distributed with a preferential representation in the lungs and skin are negatively impacted in the absence of retinoic acid receptor-related orphan receptor ..
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Grants
Awarded by NHMRC
Awarded by US Department of Defense
Awarded by National Health and Medical Research Council of Australia (NHMRC) Australia Fellowship
Awarded by National Health and Medical Research Council of Australia (NHMRC)
Awarded by NHMRC Senior Principal Research Fellowship
Awarded by Agence Nationale de la Recherche
Funding Acknowledgements
We thank Josette Fontaine, Shin-Foong Ngiow, Deborah Knight, Sebastien Fleury, Julien Wartelle and Kim Steegh for technical assistance. We thank Qerime Mundrea, Ben Venville, Jessica May, Joanne Sutton and Liam Town for maintaining and caring for the mice. We also thank the Peter MacCallum flow cytometry core facility for technical assistance. This work was supported by an NHMRC Program Grant (454569 and 1013367). CP was supported by a postdoctoral fellowship from the US Department of Defense (W81XWH-11-1-0585) and INSERM. MJS and FSFG were supported by a National Health and Medical Research Council of Australia (NHMRC) Australia Fellowship and Program Grant (1013367). MTC was supported by a Cancer Research Institute PhD scholarship. GTB was supported by an ARC Future Fellowship. FT was supported by CNRS. PN was supported by a National Health and Medical Research Council of Australia (NHMRC) Program Grant (1013367). DIG was supported by an NHMRC Senior Principal Research Fellowship (1020770). NAG was supported by a Leukaemia Foundation of Australia postgraduate scholarship. TM is supported by research grants from the Canadian Institutes of Health Research and the Crohn and Colitis Foundation of Canada, as well as a Tier 2 Canada Research Chair. NKE is a recipient of a Vanier Canada Graduate Scholarship. DAM, DS-S and DD were supported by the Agence Nationale de la Recherche (ANR-10-LABX-46) and the 'Fondation de France'.