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Immune mechanisms in pulmonary fibrosis.
Am. J. Respir. Cell Mol. Biol. 55, 309-322 (2016)
Pulmonary fibrosis, particularly idiopathic pulmonary fibrosis, represents a chronic and progressive disease with high mortality and limited therapeutic options. Excessive deposition of extracellular matrix proteins results in fibrotic remodeling, alveolar destruction and irreversible loss of lung function. Both innate and adaptive immune mechanisms contribute to fibrogenesis at several cellular and non-cellular levels. Here, we summarize and discuss the role of immune cells (T cells, neutrophils, macrophages and fibrocytes) and soluble mediators (cytokines and chemokines) involved in pulmonary fibrosis, pointing towards novel immune-based therapeutic strategies in the field.
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Scopus SNIP
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Times Cited
Times Cited
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4.082
1.029
127
136
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Publication type
Article: Journal article
Document type
Review
Keywords
T Cells ; Fibrosis ; Immunity ; Lung ; Neutrophils; Epithelial-mesenchymal Transition; Growth-factor-beta; Muc5b Promoter Polymorphism; Human Lung Fibroblasts; Regulatory T-cells; Gamma-delta T; Bronchoalveolar Lavage Fluid; Tyrosine Kinase Inhibitor; Versus-host-disease; Tgf-beta
Language
english
Publication Year
2016
HGF-reported in Year
2016
ISSN (print) / ISBN
1044-1549
e-ISSN
1535-4989
Quellenangaben
Volume: 55,
Issue: 3,
Pages: 309-322
Publisher
American Thoracic Society
Publishing Place
New York
Reviewing status
Peer reviewed
Institute(s)
Institute of Lung Health and Immunity (LHI)
POF-Topic(s)
30202 - Environmental Health
Research field(s)
Lung Research
PSP Element(s)
G-501600-001
G-505000-006
G-505000-006
WOS ID
WOS:000385984100003
PubMed ID
27149613
Erfassungsdatum
2016-05-09