The Role of TNFα and IL-17 in the Development of Excess IL-1 Signaling-Induced Inflammatory Diseases in IL-1 Receptor Antagonist-Deficient Mice

摘要: IL-1 receptor antagonist (IL-1Ra)-deficient mice spontaneously develop several inflammatory diseases, resembling rheumatoid arthritis, aortitis, and psoriasis in humans. As adoptive T cell transplantation could induce arthritis aortitis recipient mice, it was suggested that an autoimmune process is involved the development of diseases. In contrast, as dermatitis developed scid/scid-IL-1Ra-deficient not be induced by transfer, a cell-independent mechanism suggested. The expression proinflammatory cytokines augmented at sites. significantly suppressed deficiency TNFα or IL-17. also inhibited TNFα. These observations suggest IL-17 play crucial role autoimmunity downstream signaling, excess signaling-induced induces skin inflammation manner.