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In the Shadow of Fibrosis: Innate Immune Suppression Mediated by Transforming Growth Factor-β

Authors :
Philip G. Bardin
Kate L Loveland
Keiko Kan-o
Belinda J. Thomas
Jack A. Elias
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.

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