In the shadow of fibrosis: Innate immune suppression mediated by transforming growth factor-β

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

Research output: Contribution to journalReview ArticleResearchpeer-review

25 Citations (Scopus)


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 immunesuppressive actions involving both innate and adaptive responses, but often this aspect of TGFB biology is overlooked. Recent investigations have demonstrated that TGFB causes wideranging 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.

Original languageEnglish
Pages (from-to)759-766
Number of pages8
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Issue number6
Publication statusPublished - 1 Dec 2016


  • Idiopathic pulmonary fibrosis
  • Immunity
  • Lung disease
  • Transforming growth factor-β
  • Virus infection

Cite this