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In the Shadow of Fibrosis: Innate Immune Suppression Mediated by Transforming Growth Factor-β
- Source :
- American Journal of Respiratory Cell and Molecular Biology. 55:759-766
- Publication Year :
- 2016
- Publisher :
- American Thoracic Society, 2016.
-
Abstract
- Transforming growth factor-β (TGFB) regulates cell proliferation, differentiation, apoptosis, and matrix homeostasis and is intimately involved in fibrosis. TGFB expression is increased in fibrotic lung diseases, such as idiopathic pulmonary fibrosis, and in chronic inflammatory conditions, such as chronic obstructive pulmonary disease and asthma. In addition to exhibiting profibrotic activities, the protein exhibits profound immune-suppressive actions involving both innate and adaptive responses, but often this aspect of TGFB biology is overlooked. Recent investigations have demonstrated that TGFB causes wide-ranging immune suppression, including blunting of pivotal early innate IFN responses. These activities permit severe virus infections, often followed by secondary bacterial infections, which may last longer, with augmented inflammation, scarring, fibrosis, and loss of lung function. Strategies to oppose TGFB actions or to enhance IFN responses may help ameliorate the detrimental consequences of infection in patients with diseases characterized by TGFB overexpression, inflammation, and fibrosis.
- Subjects :
- 0301 basic medicine
Pulmonary and Respiratory Medicine
Pulmonary Fibrosis
Clinical Biochemistry
Inflammation
Biology
Models, Biological
03 medical and health sciences
Idiopathic pulmonary fibrosis
Immune system
Transforming Growth Factor beta
Fibrosis
Immunity
medicine
Animals
Humans
Lung
Molecular Biology
Innate immune system
Cell Biology
medicine.disease
Immunity, Innate
030104 developmental biology
medicine.anatomical_structure
Immunology
medicine.symptom
Signal Transduction
Transforming growth factor
Subjects
Details
- ISSN :
- 15354989 and 10441549
- Volume :
- 55
- Database :
- OpenAIRE
- Journal :
- American Journal of Respiratory Cell and Molecular Biology
- Accession number :
- edsair.doi.dedup.....0e9ceeda6a52b3e2a68aab7d3a9ea752
- Full Text :
- https://doi.org/10.1165/rcmb.2016-0248ps