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Nat Commun. 2017 Jun 5;8:15632. doi: 10.1038/ncomms15632.

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

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Department of Molecular &Cellular Biology, University of Adelaide, Adelaide, South Australia 5005, Australia.
Research Centre for Infectious Diseases, University of Adelaide, Adelaide, South Australia 5005, Australia.
The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia.
Department of Medical Biology, University of Melbourne, Parkville, Victoria 3010, Australia.
Department of Immunology and Infectious Diseases, John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory 2601, Australia.
Department of Internal Medicine II, University Hospital Regensburg, Regensburg 93042, Germany.
Centre for Molecular Pathology, University of Adelaide, Adelaide, South Australia 5005, Australia.


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.

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