In RA and SpA, when innate immune altered, macrophages heavily infiltrate the synovial tissues in inflammatory arthritis and also produce abundant key proinflammatory cytokines (TNF-α, IL-1, IL-23, IL-17) in the pathogenesis of RA and SpA.[6,7] There may be certain relationship between the altered innate immune responses and the nonantigen-presenting functions of HLA-B27 including the induction of UPR. This evidence concerns the gene IL17A and rheumatoid arthritis.