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Figure 1: IL-17 in SLE pathogenesis. IL-17, IL-21, and BAFF promote survival, class-switching, and production of antinuclear autoantibodies by autoreactive B cells. Consequently, nucleic acid-containing immune complexes stimulate plasmacytoid dendritic cells (pDCs) to produce type I interferon, IL-6, and IL-23, which enhance DC activation, and TH17 induction, thus completing a feedback loop for autoimmune activation. Concurrently, hyperactivation in the context of autoimmunity may actuate the accumulation of double-negative T (DNT) cells which produce more IL-17 and exacerbates the disease state. Ultimately, TH17 and DNT cells infiltrate systemic tissues and incite end organ disease.