Ontology highlight
ABSTRACT: Objective
Rheumatoid arthritis (RA) is usually preceded and likely mediated by autoantibodies to citrullinated proteins (ACPAs) that recognize citrulline residues on multiple proteins. Conversion of arginine into citrulline is performed by enzymes called peptidyl arginine deiminases (PADs). We have previously demonstrated that the human PAD4 (hPAD4) is a T cell target whose recognition provides help for the production of ACPAs by a hapten/carrier mechanism. Human PAD4 is thus an attractive therapeutic target to stop ACPA production. Here, we tested whether tolerization to hPAD4 may block the production of anti-citrullinated peptide antibodies.Methods
We used a tolerogenic plasmid encoding hPAD4 and transforming growth factor (TGF) β1, interleukin (IL) 10, and IL-2 in a mode
SUBMITTER: Pagni PP
PROVIDER: S-EPMC12854003 | biostudies-literature | 2026 Jan
REPOSITORIES: biostudies-literature