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.
|Number of pages||3|
|Journal||Nature Reviews Rheumatology|
|Early online date||14 Sep 2018|
|Publication status||Published - 1 Oct 2018|