Objective
In classic studies on the genetic background of antibody production, MHC has been shown to act as the most prominent immune-response gene that controls the magnitude and the specificity of antibody production. The strongest genetic risk factor for rheumatoid arthritis (RA), the human MHC, HLA-DRB1 shared epitope (SE) alleles, predisposes for antibodies against citrullinated proteins (ACPA). ACPA levels are higher in SE-positive than in SE-negative RA patients. The present study determines whether SE not only influences the magnitude, but also the specificity of the ACPA response.