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• W1569890859 abstract "We have previously postulated that as well as T-helper (Th) 1 and Th17 cells, the transforming growth factor (TGF)-β/fibronectin (FN)/α5β1 pathway is central to psoriasis pathogenesis. EDA+ FN refers to an alternatively spliced isoform of FN with an additional domain known as extra domain A. EDA+ FN has two important properties pertinent to psoriasis lesions: it stimulates keratinocyte hyperproliferation, and, through stimulation of Toll-like receptor (TLR) 4, stimulates production of proinflammatory cytokines. EDA+ FN production induced by TGF-β stimulation can be maintained in psoriasis lesions via two main feedback loops. Firstly, EDA+ FN stimulates proliferation of keratinocytes, which, in an autocrine fashion, will release more EDA+ FN. Secondly, EDA+ FN stimulates TLR4 expressed by antigen-presenting cells resulting in the production of proinflammatory cytokines such as tumour necrosis factor-α, interleukin (IL)-1, IL-6 and IL-12. The resultant promotion of cutaneous inflammation results in the recruitment of Th1 cells, which also produce EDA+ FN. We propose that these ‘FN loops’ contribute to the maintenance and progression of psoriatic lesions. Finally, although the association between psoriasis and heart/thrombotic disease remains unclear one plausible link may be the promotion of atherosclerosis and thrombotic heart disease by EDA+ FN." @default.
• W1569890859 created "2016-06-24" @default.
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• W1569890859 date "2010-02-27" @default.
• W1569890859 modified "2023-09-28" @default.
• W1569890859 title "Psoriasis and extra domain A fibronectin loops" @default.
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• W1569890859 doi "https://doi.org/10.1111/j.1365-2133.2010.09737.x" @default.
• W1569890859 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20192957" @default.
• W1569890859 hasPublicationYear "2010" @default.
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