| First Author | McKenzie DR | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Pages | 15632 | PubMed ID | 28580944 |
| Mgi Jnum | J:250341 | Mgi Id | MGI:5921949 |
| Doi | 10.1038/ncomms15632 | Citation | McKenzie DR, et al. (2017) IL-17-producing gammadelta T cells switch migratory patterns between resting and activated states. Nat Commun 8:15632 |
| abstractText | Interleukin 17-producing gammadelta T (gammadeltaT17) cells have unconventional trafficking characteristics, residing in mucocutaneous tissues but also homing into inflamed tissues via circulation. Despite being fundamental to gammadeltaT17-driven early protective immunity and exacerbation of autoimmunity and cancer, migratory cues controlling gammadeltaT17 cell positioning in barrier tissues and recruitment to inflammatory sites are still unclear. Here we show that gammadeltaT17 cells constitutively express chemokine receptors CCR6 and CCR2. While CCR6 recruits resting gammadeltaT17 cells to the dermis, CCR2 drives rapid gammadeltaT17 cell recruitment to inflamed tissues during autoimmunity, cancer and infection. Downregulation of CCR6 by IRF4 and BATF upon gammadeltaT17 activation is required for optimal recruitment of gammadeltaT17 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 gammadeltaT17 cells to inflammatory lesions. |
