Background. γδ T cells play a key role in the regulation of inflammatory responses in epithelial tissue, and in adaptive immunity, as γδ T cell deficient mice have a severely impaired capacity to clear lung pathogens. γδ T cells regulate the initial inflammatory response to microbial invasion and thereby protect against tissue injury. Here we examined the response of γδ 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 γδ T cells to the lung lesions. γδ T cells were the predominant source of IL-17 (as detected by flow cytometry and real-time PCR). Moreover, γδ 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 γδ T cells produce IL-17 in response to lung injury and are required for an organized inflammatory response and epithelial repair. The lack of γδ T cells correlates with increased inflammation and fibrosis. © 2008 Springer Science+Business Media, LLC.
CITATION STYLE
Braun, R. K., Ferrick, C., Neubauer, P., Sjoding, M., Sterner-Kock, A., Kock, M., … Love, R. B. (2008). IL-17 producing γδ T cells are required for a controlled inflammatory response after bleomycin-induced lung injury. Inflammation, 31(3), 167–179. https://doi.org/10.1007/s10753-008-9062-6
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