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    IL-17-producing gamma delta Tcells switch migratory patterns between resting and activated states

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    Author
    McKenzie, DR; Kara, EE; Bastow, CR; Tyllis, TS; Fenix, KA; Gregor, CE; Wilson, JJ; Babb, R; Paton, JC; Kallies, A; ...
    Date
    2017-06-05
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Kallies, Axel; Nutt, Stephen
    Affiliation
    Medical Biology (W.E.H.I.)
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    McKenzie, D. R., Kara, E. E., Bastow, C. R., Tyllis, T. S., Fenix, K. A., Gregor, C. E., Wilson, J. J., Babb, R., Paton, J. C., Kallies, A., Nutt, S. L., Brustle, A., Mack, M., Comerford, I. & McColl, S. R. (2017). IL-17-producing gamma delta Tcells switch migratory patterns between resting and activated states. NATURE COMMUNICATIONS, 8 (1), https://doi.org/10.1038/ncomms15632.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256209
    DOI
    10.1038/ncomms15632
    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.

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