title: Dermal-resident versus recruited γδ T cell response to cutaneous vaccinia virus infection.
abstract: The study of T cell immunity at barrier surfaces has largely focused on T cells bearing the αβ TCR. However, T cells that express the γδ TCR are disproportionately represented in peripheral tissues of mice and humans, suggesting they too may play an important role responding to external stimuli. In this article, we report that, in a murine model of cutaneous infection with vaccinia virus, dermal γδ T cell numbers increased 10-fold in the infected ear and resulted in a novel γδ T cell population not found in naive skin. Circulating γδ T cells were specifically recruited to the site of inflammation and differentially contributed to dermal populations based on their CD27 expression. Recruited γδ T cells, the majority of which were CD27(+), were granzyme B(+) and made up about half of the dermal population at the peak of the response. In contrast, recruited and resident γδ T cell populations that made IL-17 were CD27(-). Using a double-chimera model that can discriminate between the resident dermal and recruited γδ T cell populations, we demonstrated their divergent functions and contributions to early stages of tissue inflammation. Specifically, the loss of the perinatal thymus-derived resident dermal population resulted in decreased cellularity and collateral damage in the tissue during viral infection. These findings have important implications for our understanding of immune coordination at barrier surfaces and the contribution of innate-like lymphocytes on the front lines of immune defense.
authors.affiliation: Department of Immunology, University of Washington, Seattle, WA 98109;
authors.forename: Amanda S
authors.initials: AS
authors.lastname: Woodward Davis
authors.affiliation: Department of Immunology, University of Washington, Seattle, WA 98109; Howard Hughes Medical Institute, University of Washington, Seattle, WA 98109; and.
authors.forename: Tessa
authors.initials: T
authors.lastname: Bergsbaken
authors.affiliation: Department of Comparative Medicine, University of Washington, Seattle, WA 98109.
authors.forename: Martha A
authors.initials: MA
authors.lastname: Delaney
authors.affiliation: Department of Immunology, University of Washington, Seattle, WA 98109; Howard Hughes Medical Institute, University of Washington, Seattle, WA 98109; and mbevan@uw.edu.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Bevan
mesh_terms: D000818:Animals; D002465:Cell Movement; D002678:Chimera / Q000276:immunology / Q000821:virology; D020405:Dermis / Q000276:immunology* / Q000473:pathology / Q000821:virology; D004423:Ear / Q000473:pathology / Q000821:virology*; D005786:Gene Expression Regulation; D053804:Granzymes / Q000235:genetics / Q000276:immunology; D007113:Immunity, Innate; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology; D008198:Lymph Nodes / Q000276:immunology / Q000473:pathology / Q000821:virology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011213:Poxviridae Infections / Q000276:immunology* / Q000473:pathology / Q000821:virology; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics / Q000276:immunology*; D015398:Signal Transduction; D013154:Spleen / Q000276:immunology / Q000473:pathology / Q000821:virology; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology / Q000821:virology; D013950:Thymus Gland / Q000276:immunology / Q000473:pathology / Q000821:virology; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000235:genetics / Q000276:immunology; D014616:Vaccinia virus / Q000276:immunology*
chemical_list: D020381:Interleukin-17; D016692:Receptors, Antigen, T-Cell, gamma-delta; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7; D053804:Granzymes; C509214:Gzmb protein, mouse