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Dermal γδ T Cells Do Not Freely Re-Circulate Out of Skin and Produce IL-17 to Promote Neutrophil Infiltration during Primary Contact Hypersensitivity

Authors
 Xiaodong Jiang  ;  Chang Ook Park  ;  Jenna Geddes Sweeney  ;  Min Jae Yoo  ;  Olivier Gaide  ;  Thomas Seth Kupper 
Citation
 PLOS ONE, Vol.12(1) : e0169397, 2017 
Journal Title
 PLOS ONE 
Issue Date
2017
MeSH
Animals ; Dermatitis, Contact/genetics ; Dermatitis, Contact/immunology* ; Dermatitis, Contact/pathology ; Dermis/immunology* ; Dermis/pathology ; Interleukin-17/genetics ; Interleukin-17/immunology* ; Interleukins/genetics ; Interleukins/immunology ; Mice ; Mice, Knockout ; Neutrophil Infiltration* ; Neutrophils/immunology* ; Neutrophils/pathology ; Receptors, Antigen, T-Cell, gamma-delta/genetics ; Receptors, Antigen, T-Cell, gamma-delta/immunology* ; T-Lymphocytes/immunology* ; T-Lymphocytes/pathology
Abstract
The role of mouse dermal γδ 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 γδ T cell receptor (TCR) and reside in murine epidermis from birth. We asked if dermal γδ cells freely re-circulated out of skin, or behaved more like dermal resident memory T cells (TRM) in mice. We found that, unlike epidermal γδ T cells (DETC), dermal γδ 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 γδ T cells re-circulate very slowly—more rapidly than authentic αβ TCR TRM, but more slowly than the recently described dermal αβ TCR T migratory memory cells (TMM). Mice lacking the TCR δ gene (δ-/-) had a significant reduction of 2,4-dinitrofluorobenzene (DNFB)-induced contact hypersensitivity (CHS). We created mice deficient in dermal γδ 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 γδ 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 Vγ4+ 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 γδ 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.
Files in This Item:
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DOI
10.1371/journal.pone.0169397
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
Yonsei Authors
Park, Chang Ook(박창욱) ORCID logo https://orcid.org/0000-0003-3856-1201
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/154658
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