The addition of IL-27 into IL-23-induced arthritis mice ameliorated disease incidence and disease severity, inhibited neutrophil proliferation and γδ T-cell accumulation, and resulted in reduction in serum levels of IL-6, IL-17, and IgG2a, and percentage of cells expressing IL-17 and IFNγ (180, 181). This evidence concerns the gene IL17A and arthritic joint disease.