Anti-carbamylated protein antibodies drive AEC II toward a profibrotic phenotype by interacting with carbamylated TLR5
Authors' conclusion
Overall, we found anti-CarP drives aberrant AEC II activation by interacting with carbamylated TLR5 to promote ILD progression.
Study context
- Population
- Serum samples from patients with CTD with and without interstitial lung disease (ILD); male C57BL/6 micemice n = 5
- Participants
- 89 vs 170
- Comparison
- CTD with ILD vs CTD without ILD; Anti-carbamylated protein (anti-CarP) treatment in mice and AEC II
- CTD-ILDn = 89
- non-CTD-ILDn = 170reference
- Outcome
- Role of anti-CarP antibodies in lung fibrosis in CTD-ILD (serum anti-CarP level; mechanistic effects in vivo and in AEC II)
Methodological detailsELISA of human serum, mouse pulmonary fibrosis model, in vitro cell treatment
- ELISA of human serum
- Mouse pulmonary fibrosis model
- In vitro cell treatment
Main finding
As reported in the abstract
Lysine carbamylation sites in TLR5 ectodomain, allowing anti-CarP interaction with carbamylated TLR5
up to 12
Original publication
Anti-carbamylated protein antibodies drive AEC II toward a profibrotic phenotype by interacting with carbamylated TLR5. Rheumatology (Oxford). Published 16 February 2024. doi:10.
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