Role of IL-17A in murine models of COPD airway disease
| العنوان: | Role of IL-17A in murine models of COPD airway disease |
|---|---|
| المؤلفون: | Saburo Ito, Amanda Goodsell, Naoki Takasaka, Mitsuo Hashimoto, Jody L. Baron, Haruhiko Yanagisawa, Stephen L. Nishimura, Shunsuke Minagawa, Catherine Moermans, Royce Ma, Alison L. Budelsky, Jun Araya |
| المصدر: | American journal of physiology. Lung cellular and molecular physiology, vol 312, iss 1 Yanagisawa, H; Hashimoto, M; Minagawa, S; Takasaka, N; Ma, R; Moermans, C; et al.(2016). Role of Il-17A in murine models of COPD airway disease. American Journal of Physiology-Lung Cellular and Molecular Physiology, 312(1), L122-L130. doi: 10.1152/ajplung.00301.2016. UCSF: Retrieved from: http://www.escholarship.org/uc/item/5c63d8ttTest |
| بيانات النشر: | American Physiological Society, 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | 0301 basic medicine, Physiology, Pulmonary Fibrosis, Respiratory System, Medical Physiology, Interleukin-1beta, Inbred C57BL, interleukin-17, Mice, Pulmonary Disease, Chronic Obstructive, 0302 clinical medicine, Fibrosis, Receptors, Pulmonary fibrosis, 2.1 Biological and endogenous factors, Lung, COPD, Receptors, Interleukin-17, cigarette smoke, Innate lymphoid cell, Interleukin-17, Smoking, respiratory system, Respiratory, Interleukin 17, medicine.symptom, Research Article, Pulmonary and Respiratory Medicine, Chronic Obstructive, Chronic Obstructive Pulmonary Disease, Inflammation, Adenoviridae, Pulmonary Disease, 03 medical and health sciences, Neutralization Tests, Physiology (medical), medicine, Animals, Animal, business.industry, fibrosis, Cell Biology, Pneumonia, medicine.disease, respiratory tract diseases, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Poly I-C, 030228 respiratory system, airway, inflammation, Disease Models, Immunology, Airway, business, CD8 |
| الوصف: | © 2017 the American Physiological Society. Small airway fibrosis is a major pathological feature of chronic obstructive pulmonary disease (COPD) and is refractory to current treatments. Chronic inflammatory cells accumulate around small airways in COPD and are thought to play a major role in small airway fibrosis. Mice deficient in α/β T cells have recently been shown to be protected from both experimental airway inflammation and fibrosis. In these models, CD4+Th17 cells and secretion of IL-17A are increased. However, a pathogenic role for IL-17 in specifically mediating fibrosis around airways has not been demonstrated. Here a role for IL-17A in airway fibrosis was demonstrated using mice deficient in the IL-17 receptor A (il17ra). Il17ra-deficient mice were protected from both airway inflammation and fibrosis in two different models of airway fibrosis that employ COPD-relevant stimuli. In these models, CD4+ Th17 are a major source of IL-17A with other expressing cell types including γδ T cells, type 3 innate lymphoid cells, polymorphonuclear cells, and CD8+ T cells. Antibody neutralization of IL-17RA or IL-17A confirmed that IL-17A was the relevant pathogenic IL-17 isoform and IL-17RA was the relevant receptor in airway inflammation and fibrosis. These results demonstrate that the IL-17A/IL-17 RA axis is crucial to murine airway fibrosis. These findings suggest that IL-17 might be targeted to prevent the progression of airway fibrosis in COPD. |
| وصف الملف: | application/pdf |
| اللغة: | English |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::037918cdf8d43f9f1b498320a3a7539aTest https://europepmc.org/articles/PMC5283930Test/ |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....037918cdf8d43f9f1b498320a3a7539a |
| قاعدة البيانات: | OpenAIRE |
| الوصف غير متاح. |