In addition, the TLR3 agonist poly(I:C) upregulated not only IFNβ, but IFNλ1 and IFNλ2 expression in the FLS from JIA patients suggesting that FLS can also produce both type I and type III IFNs and likely contribute to the inflammatory environment in the joint. This evidence concerns the gene TLR3 and juvenile idiopathic arthritis.