In addition, we have previously proposed a mechanism for generation of Th17 cells in the joint itself, as cell contact with in vitro (LPS) activated [36] or in vivo activated monocytes from inflamed joints from RA patients [11] leads to induction of IL-17 production in memory CD4+ T cells, suggesting that newly recruited CD4+ T cells can be skewed toward a Th17 phenotype at the site of inflammation. Here, CD4 is linked to rheumatoid arthritis.