Because these cytokines are never released by activated FLSs, the present data suggest that FLSs may play an important role in the amplification of inflammatory reactions in RA, by expressing IL-32, which in turn induces the expression of TNF-α, IL-1, or IL-18 by macrophages or dendritic cells, bridging innate and adaptive immunity. Here, TNF is linked to rheumatoid arthritis.