Rheumatoid arthritis (RA) is a T cell mediated autoimmune disease and associated with HLA-DR4 or HLA-DR1 subtypes.^1,2 Type II collagen (CII) has been implicated as an autoantigen of RA, and CD4+ T cell responses to CII or CII derived peptides are mainly presented by HLA-DR4/1 molecules.^3,4 Inhibition of antigen presentation by HLA-DR4/1 molecules can interfere with T cell mediated autoimmune responses in RA.

Our previous studies have suggested that altered CII263–272 peptides inhibited CII263–272-induced T cell activation by blocking antigen presentation.^5,6 In this study we examine the role of the altered influenza virus haemagglutinin (HA) 308–317 peptides (altered peptide ligands (APLs)) with single or multiple substitutions of T cell receptor (TCR) contact residues in T cell responses of peripheral blood mononuclear cells (PBMC) and inhibitory effects of APLs on CII263–272-induced T cell activation in RA.

Twenty seven HLA-DR4/1 positive patients with RA (21 female, 6 male; mean (SD) age 53.6 …