Hams E, Armstrong ME, Barlow JL, Saunders SP, Schwartz C, Cooke G, Fahy RJ, Crotty TB, Hirani N, Flynn RJ, Vöhringer D, Mckenzie ANJ, Donnelly SC, Fallon PG (2014)
Publication Type: Journal article
Publication year: 2014
Publisher: National Academy of Sciences
Book Volume: 111
Pages Range: 367-72
Journal Issue: 1
Disease conditions associated with pulmonary fibrosis are progressive and have a poor long-term prognosis with irreversible changes in airway architecture leading to marked morbidity and mortalities. Using murine models we demonstrate a role for interleukin (IL)-25 in the generation of pulmonary fibrosis. Mechanistically, we identify IL-13 release from type 2 innate lymphoid cells (ILC2) as sufficient to drive collagen deposition in the lungs of challenged mice and suggest this as a potential mechanism through which IL-25 is acting. Additionally, we demonstrate that in human idiopathic pulmonary fibrosis there is increased pulmonary expression of IL-25 and also observe a population ILC2 in the lungs of idiopathic pulmonary fibrosis patients. Collectively, we present an innate mechanism for the generation of pulmonary fibrosis, via IL-25 and ILC2, that occurs independently of T-cell-mediated antigen-specific immune responses. These results suggest the potential of therapeutically targeting IL-25 and ILC2 for the treatment of human fibrotic diseases.
APA:
Hams, E., Armstrong, M.E., Barlow, J.L., Saunders, S.P., Schwartz, C., Cooke, G.,... Fallon, P.G. (2014). IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis. Proceedings of the National Academy of Sciences of the United States of America, 111(1), 367-72. https://doi.org/10.1073/pnas.1315854111
MLA:
Hams, Emily, et al. "IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis." Proceedings of the National Academy of Sciences of the United States of America 111.1 (2014): 367-72.
BibTeX: Download