Systemic sclerosis & Raynaud's
TLR8 aggravates skin inflammation and fibrosis by activating skin fibroblasts in systemic sclerosis
An erratum to this article was published (Rheumatology (Oxford), 3 May 2024 ↗)
Authors' conclusion
TLR8 might be a promising therapeutic target for improving the treatment strategy for skin inflammation and fibrosis in SSc.
Study context
- Population
- Skin tissues and skin fibroblasts of SSc patients; Bleomycin (BLM)-induced mouse model
- Outcome
- Expression, mechanism and pathogenic role of TLR8 in SSc
Methodological detailspublic dataset analysis, in vitro skin fibroblast studies, BLM-induced mouse skin inflammation and fibrosis model
- Public dataset analysis
- In vitro skin fibroblast studies
- BLM-induced mouse skin inflammation and fibrosis model
Main finding
As reported in the abstract
- TLR8 levels significantly elevated in SSc skin tissues and myofibroblasts, with significant activation of the TLR8 pathway
- TLR8 overexpression or activation (plasmid or VTX-2337) upregulated IL-6, IL-1β, COL I, COL III and α-SMA in skin fibroblasts
- TLR8-siRNA and cu-cpt-8m reversed the phenotypes of TLR8-activating fibroblasts
- TLR8 induces skin fibrosis and inflammation dependent on MAPK, NF-κB and SMAD2/3 pathways
- Subcutaneous cu-cpt-8m significantly alleviated BLM-induced skin inflammation and fibrosis in vivo
Original publication
TLR8 aggravates skin inflammation and fibrosis by activating skin fibroblasts in systemic sclerosis. Rheumatology (Oxford). Published 4 September 2023. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →