IL-17-producing γδ T cells switch migratory patterns between resting and activated states

Duncan R. McKenzie, Ervin E. Kara, Cameron R. Bastow, Timona S. Tyllis, Kevin A. Fenix, Carly E. Gregor, Jasmine J. Wilson, Rachelle Babb, James C. Paton, Axel Kallies, Stephen L. Nutt, Anne Brüstle, Matthias Mack, Iain Comerford () and Shaun R. McColl ()
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Duncan R. McKenzie: University of Adelaide
Ervin E. Kara: University of Adelaide
Cameron R. Bastow: University of Adelaide
Timona S. Tyllis: University of Adelaide
Kevin A. Fenix: University of Adelaide
Carly E. Gregor: University of Adelaide
Jasmine J. Wilson: University of Adelaide
Rachelle Babb: University of Adelaide
James C. Paton: University of Adelaide
Axel Kallies: The Walter and Eliza Hall Institute of Medical Research
Stephen L. Nutt: The Walter and Eliza Hall Institute of Medical Research
Anne Brüstle: John Curtin School of Medical Research, Australian National University
Matthias Mack: University Hospital Regensburg
Iain Comerford: University of Adelaide
Shaun R. McColl: University of Adelaide

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Interleukin 17-producing γδ T (γδT17) cells have unconventional trafficking characteristics, residing in mucocutaneous tissues but also homing into inflamed tissues via circulation. Despite being fundamental to γδT17-driven early protective immunity and exacerbation of autoimmunity and cancer, migratory cues controlling γδT17 cell positioning in barrier tissues and recruitment to inflammatory sites are still unclear. Here we show that γδT17 cells constitutively express chemokine receptors CCR6 and CCR2. While CCR6 recruits resting γδT17 cells to the dermis, CCR2 drives rapid γδT17 cell recruitment to inflamed tissues during autoimmunity, cancer and infection. Downregulation of CCR6 by IRF4 and BATF upon γδT17 activation is required for optimal recruitment of γδT17 cells to inflamed tissue by preventing their sequestration into uninflamed dermis. These findings establish a lymphocyte trafficking model whereby a hierarchy of homing signals is prioritized by dynamic receptor expression to drive both tissue surveillance and rapid recruitment of γδT17 cells to inflammatory lesions.

Date: 2017
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DOI: 10.1038/ncomms15632

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