Additionally, a cell culture model using primary human bronchial epithelial (HBE) cells showed that IL-17 stimulation caused reductions in IFNλ1–3 production during influenza infection and in mice, treatment with IFNλ2 reduced IL-17-producing Th17 and γδ T cells in a model of collagen-induced arthritis [42,65]. Here, IFNL1 is linked to influenza.