The role of B cells in immunopathogenesis of RA has not been fully characterised but several possible mechanisms of action have been proposed; B cells may function as antigen presenting cells with co-stimulatory signals required for T cells CD4 regulation, as well they may secrete proinflammatory cytokines (TNF, IL6, other chemokines) and regulate immune response during RA contributing to the inflammation and bone erosions. This evidence concerns the gene CD4 and rheumatoid arthritis.