| First Author | Jiang X | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 1 | Pages | e0169397 |
| PubMed ID | 28081153 | Mgi Jnum | J:248061 |
| Mgi Id | MGI:5917642 | Doi | 10.1371/journal.pone.0169397 |
| Citation | Jiang X, et al. (2017) Dermal gammadelta T Cells Do Not Freely Re-Circulate Out of Skin and Produce IL-17 to Promote Neutrophil Infiltration during Primary Contact Hypersensitivity. PLoS One 12(1):e0169397 |
| abstractText | The role of mouse dermal gammadelta T cells in inflammatory skin disorders and host defense has been studied extensively. It is known that dendritic epidermal T cells (DETC) have a monomorphic gammadelta T cell receptor (TCR) and reside in murine epidermis from birth. We asked if dermal gammadelta cells freely re-circulated out of skin, or behaved more like dermal resident memory T cells (TRM) in mice. We found that, unlike epidermal gammadelta T cells (DETC), dermal gammadelta cells are not homogeneous with regard to TCR, express the tissue resident T cell markers CD69 and CD103, bear skin homing receptors, and produce IL-17 and IL-22. We created GFP+: GFP- parabiotic mice and found that dermal gammadelta T cells re-circulate very slowly-more rapidly than authentic alphabeta TCR TRM, but more slowly than the recently described dermal alphabeta TCR T migratory memory cells (TMM). Mice lacking the TCR delta gene (delta-/-) had a significant reduction of 2,4-dinitrofluorobenzene (DNFB)-induced contact hypersensitivity (CHS). We created mice deficient in dermal gammadelta T cells but not DETC, and these mice also showed a markedly reduced CHS response after DNFB challenge. The infiltration of effector T cells during CHS was not reduced in dermal gammadelta T cell-deficient mice; however, infiltration of Gr-1+CD11b+ neutrophils, as well as ear swelling, was reduced significantly. We next depleted Gr-1+ neutrophils in vivo, and demonstrated that neutrophils are required for ear swelling, the accepted metric for a CHS response. Depletion of IL-17-producing dermal Vgamma4+ cells and neutralization of IL-17 in vivo, respectively, also led to a significantly reduced CHS response and diminished neutrophil infiltration. Our findings here suggest that dermal gammadelta T cells have an intermediate phenotype of T cell residence, and play an important role in primary CHS through producing IL-17 to promote neutrophil infiltration. |
