title: Activated skin γδ T-cells regulate T-cell infiltration of the wound site after burn.
abstract: Burn induces an immunopathological response involving multiple immune cell types that includes γδ T-cells. Nonetheless, the role of γδ T-cells at the wound site after burn is not clearly defined. Wild type and γδ T-cell receptor deficient (δ TCR(-/-)) mice were subjected to a major burn or sham procedure. At 1-7 d thereafter, skin samples were collected and T-cell populations analyzed. The majority of T-cells in the skin of sham mice were γδ T-cells. After burn, however, an increase in the total T-cells was observed at the wound site and these cells were predominantly αβ T-cells. Their influx was γδ T-cell dependent, as it was markedly reduced in injured δ TCR(-/-) mice. Burn wound γδ T-cells were activated with increased expression of TLRs and CD69. In contrast, the infiltrating αβ T-cells TLR and CD69 expressions were attenuated after burn. Thus, burn is associated with of γδ T-cell activation at the injury site, which initiates a massive infiltration of the wound with αβ T-cells that likely facilitate the transition from the inflammatory to the proliferative phase of healing.
authors.affiliation: Department of Surgery, The University of Texas Health Science Center, San Antonio, TX, USA.
authors.forename: Meenakshi
authors.initials: M
authors.lastname: Rani
authors.affiliation: Department of Surgery, The University of Texas Health Science Center, San Antonio, TX, USA.
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: US Army Institute of Surgical Research, Fort Sam Houston, TX, USA.
authors.forename: Michael R
authors.initials: MR
authors.lastname: Scherer
authors.affiliation: Department of Surgery, The University of Texas Health Science Center, San Antonio, TX, USA US Army Institute of Surgical Research, Fort Sam Houston, TX, USA.
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Cap
authors.affiliation: Department of Surgery, The University of Texas Health Science Center, San Antonio, TX, USA US Army Institute of Surgical Research, Fort Sam Houston, TX, USA schwacha@uthscsa.edu.
authors.forename: Martin G
authors.initials: MG
authors.lastname: Schwacha
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D002056:Burns / Q000276:immunology*; D002465:Cell Movement / Q000235:genetics / Q000276:immunology; D004195:Disease Models, Animal; D006801:Humans; D037181:Lectins, C-Type / Q000378:metabolism; D008213:Lymphocyte Activation; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000378:metabolism; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics / Q000378:metabolism; D012867:Skin / Q000276:immunology* / Q000293:injuries; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D051193:Toll-Like Receptors / Q000378:metabolism; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D037181:Lectins, C-Type; D016693:Receptors, Antigen, T-Cell, alpha-beta; D016692:Receptors, Antigen, T-Cell, gamma-delta; D051193:Toll-Like Receptors; D000099192:CD69 Antigens
keywords: CD69; Injury; Toll-like receptors; inflammation; trauma