PropertyValue
?:abstract
  • Interleukin (IL)-11 evolved as part of the innate immune response. In the human lung, IL-11 upregulation has been associated with viral infections and a range of fibroinflammatory diseases, including idiopathic pulmonary fibrosis. Transforming growth factor-beta (TGFβ) and other disease factors can initiate an autocrine loop of IL-11 signaling in pulmonary fibroblasts, which, in a largely ERK-dependent manner, triggers the translation of profibrotic proteins. Lung epithelial cells also express the IL-11 receptor and transition into a mesenchymal-like state in response to IL-11 exposure. In mice, therapeutic targeting of IL-11 with antibodies can arrest and reverse bleomycin-induced pulmonary fibrosis and inflammation. Intriguingly, fibroblast-specific blockade of IL-11 signaling has anti-inflammatory effects, which suggests that lung inflammation is sustained, in part, through IL-11 activity in the stroma. Proinflammatory fibroblasts and their interaction with the damaged epithelium may represent an important but overlooked driver of lung disease. Initially thought of as a protective cytokine, IL-11 is now increasingly recognized as an important determinant of lung fibrosis, inflammation, and epithelial dysfunction.
is ?:annotates of
?:creator
?:doi
  • 10.1038/s12276-020-00531-5
?:doi
?:journal
  • Exp_Mol_Med
?:license
  • cc-by
?:pdf_json_files
  • document_parses/pdf_json/6e69c7903777623a8644482b564aac55c9fe3460.json
?:pmc_json_files
  • document_parses/pmc_json/PMC7705429.xml.json
?:pmcid
?:pmid
?:pmid
  • 33262481.0
?:publication_isRelatedTo_Disease
?:sha_id
?:source
  • Medline; PMC
?:title
  • Interleukin-11 signaling underlies fibrosis, parenchymal dysfunction, and chronic inflammation of the airway
?:type
?:year
  • 2020-12-01

Metadata

Anon_0  
expand all