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IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis.
- Source :
- Proceedings of the National Academy of Sciences of the United States of America; 1/7/2014, Vol. 111 Issue 1, p367-372, 6p
- Publication Year :
- 2014
-
Abstract
- 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. [ABSTRACT FROM AUTHOR]
- Subjects :
- IDIOPATHIC pulmonary fibrosis
LABORATORY mice
ANTIGENS
T cells
IMMUNE response
Subjects
Details
- Language :
- English
- ISSN :
- 00278424
- Volume :
- 111
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Proceedings of the National Academy of Sciences of the United States of America
- Publication Type :
- Academic Journal
- Accession number :
- 93610730
- Full Text :
- https://doi.org/10.1073/pnas.1315854111