IL-17 producing gammadelta T cells are required for a controlled inflammatory response after bleomycin-induced lung injury. Inflammation 2008 Jun;31(3):167-79
Date
03/14/2008Pubmed ID
18338242DOI
10.1007/s10753-008-9062-6Scopus ID
2-s2.0-43349089429 (requires institutional sign-in at Scopus site) 113 CitationsAbstract
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.
CONCLUSION: 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.
Author List
Braun RK, Ferrick C, Neubauer P, Sjoding M, Sterner-Kock A, Kock M, Putney L, Ferrick DA, Hyde DM, Love RBMESH terms used to index this publication - Major topics in bold
AnimalsBleomycin
Cell Proliferation
Collagen
Disease Models, Animal
Flow Cytometry
Interleukin-17
Interleukin-6
Lung
Lymphocyte Subsets
Mice
Mice, Inbred C57BL
Mice, Knockout
Pneumonia
Pulmonary Fibrosis
Receptors, Antigen, T-Cell, gamma-delta
Respiratory Mucosa
Reverse Transcriptase Polymerase Chain Reaction
T-Lymphocytes
Time Factors