Likewise, it has been described that VIP counteracts the stimulatory effect of pro-inflammatory mediators, including TLR3 and TLR4 ligands, TNF-α, and IL-17, on the expression of IL-17 receptors and the IL-12 family of cytokines in RA-SF, which, in turn, mediates their cross-talk with Th1/Th17 cells [207]. Here, TLR3 is linked to rheumatoid arthritis.