Abstract
Inappropriate activation of Toll-like receptor 4 (TLR4) on resident fibroblasts, through the binding of damage-associated molecular patterns, is a potential driver of fibrosis in systemic sclerosis. New evidence suggests that targeting fibroblast-specific TLR4 or an accessory molecule MD2 could have therapeutic value.
Original language | English |
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Article number | e98850 |
Pages (from-to) | 564-566 |
Number of pages | 3 |
Journal | Nature Reviews. Rheumatology |
Volume | 14 |
Issue number | 10 |
DOIs | |
Publication status | Published - Oct 2018 |
Keywords
- Fibroblasts
- Fibrosis
- Humans
- Lipopolysaccharides
- Scleroderma, Systemic
- Skin
- Toll-Like Receptor 4