title: IL-17 producing gammadelta T cells are required for a controlled inflammatory response after bleomycin-induced lung injury.
abstract: BACKGROUND
  gammadelta T cells play a key role in the regulation of inflammatory responses in epithelial tissue, and in adaptive immunity, as gammadelta T cell deficient mice have a severely impaired capacity to clear lung pathogens. gammadelta T cells regulate the initial inflammatory response to microbial invasion and thereby protect against tissue injury. Here we examined the response of gammadelta T cells to lung injury induced by bleomycin, in an effort to study the inflammatory response in the absence of any adaptive immune response to a pathogen.
  
  
  RESULTS
  After lung injury by bleomycin, we localized the gammadelta T cells to the lung lesions. gammadelta T cells were the predominant source of IL-17 (as detected by flow cytometry and real-time PCR). Moreover, gammadelta T cell knockout mice showed a significant reduction in cellular infiltration into the airways, reduced expression of IL-6 in the lung, and a significant delay in epithelial repair.
  
  
  CONCLUSIONS
  Mouse gammadelta T cells produce IL-17 in response to lung injury and are required for an organized inflammatory response and epithelial repair. The lack of gammadelta T cells correlates with increased inflammation and fibrosis.
authors.affiliation: Department of Thoracic and CV Surgery, Loyola University, Maywood, Illinois, USA. rubraun@lumc.edu
authors.forename: Ruedi K
authors.initials: RK
authors.lastname: Braun
authors.forename: Christina
authors.initials: C
authors.lastname: Ferrick
authors.forename: Paul
authors.initials: P
authors.lastname: Neubauer
authors.forename: Michael
authors.initials: M
authors.lastname: Sjoding
authors.forename: Anja
authors.initials: A
authors.lastname: Sterner-Kock
authors.forename: Martin
authors.initials: M
authors.lastname: Kock
authors.forename: Lei
authors.initials: L
authors.lastname: Putney
authors.forename: David A
authors.initials: DA
authors.lastname: Ferrick
authors.forename: Dallas M
authors.initials: DM
authors.lastname: Hyde
authors.forename: Robert B
authors.initials: RB
authors.lastname: Love
mesh_terms: D000818:Animals; D001761:Bleomycin; D049109:Cell Proliferation; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D005434:Flow Cytometry; D020381:Interleukin-17 / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D008168:Lung / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016131:Lymphocyte Subsets / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011014:Pneumonia / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D020545:Respiratory Mucosa / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000276:immunology*; D013997:Time Factors
chemical_list: D020381:Interleukin-17; D015850:Interleukin-6; D016692:Receptors, Antigen, T-Cell, gamma-delta; D001761:Bleomycin; D003094:Collagen