The reduction of this inflammatory status exerted by CTLA4-Ig in RA macrophages seems to occur through a rapid downregulation of specific markers of M1 phenotype (CD80, CD86, and TLR4) and the reduction of specific pro-inflammatory cytokines (IL-6, IL-1β, and TNFα), followed by the upregulation of specific markers of anti-inflammatory M2 phenotype (CD163, CD204, CD206, and MerTK). Here, CD86 is linked to rheumatoid arthritis.