title: Dendritic epidermal T cells regulate skin homeostasis through local production of insulin-like growth factor 1.
abstract: A fine balance between rates of proliferation and apoptosis in the skin provides a defensive barrier and a mechanism for tissue repair after damage. Vgamma3(+) dendritic epidermal T cells (DETCs) are primary modulators of skin immune responses. Here we show that DETCs both produce and respond to insulin-like growth factor 1 (IGF-1) after T cell receptor stimulation. Mice deficient in DETCs had a notable increase in epidermal apoptosis that was abrogated by the addition of DETCs or IGF-1. Furthermore, DETC-deficient mice had reduced IGF-1 receptor activation at wound sites. These findings indicate critical functions for DETC-mediated IGF-1 production in regulating skin homeostasis and repair.
authors.affiliation: Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA.
authors.forename: Leslie L
authors.initials: LL
authors.lastname: Sharp
authors.forename: Julie M
authors.initials: JM
authors.lastname: Jameson
authors.forename: Gabrielle
authors.initials: G
authors.lastname: Cauvi
authors.forename: Wendy L
authors.initials: WL
authors.lastname: Havran
mesh_terms: D000818:Animals; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology*; D000078404:Epidermal Cells; D004817:Epidermis / Q000276:immunology; D006706:Homeostasis / Q000276:immunology*; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017526:Receptor, IGF Type 1; D012867:Skin / Q000293:injuries; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000502:physiology*; D014945:Wound Healing
chemical_list: D007334:Insulin-Like Growth Factor I; D017526:Receptor, IGF Type 1