The collagen type II (CII) 263–272 peptide is a predominant T and B cell antigenic peptide in rheumatoid arthritis.¹ Crystallographic data showed that 263F and 264K of CII263–272 are mainly responsible for binding with HLA-DR, and that 267Q and 270K were the major T cell receptor (TCR)-contact residues.^2,3 We have shown that the CII altered peptide ligand (APL) with individual or consecutive substitutions of the TCR-contact amino acids could inhibit T cell activation induced by wild-type CII peptide in the context of HLA-DRB1, among which the most potent T cell activation suppressor is sub268–270, in which the amino acids of wild-type CII263–272 at positions 268, 269 and 270 were substituted with glycine or alanine (FKGEQAGAGE, substitutions underlined).^4,5 Collagen-induced arthritis (CIA) is induced by wild-type CII in susceptible rodent strains. …