IL-17 is the hallmark cytokine for the newly identified subset of T helper cells, Th17. Th17 cells are important instigators of inflammation in several models of autoimmune disease; in particular, collagen induced arthritis (CIA) and experimental autoimmune encephalomyelitis (EAE), which were previously characterized as Th1-mediated diseases. Although high levels of IFN-γ are secreted in CIA and EAE, disease is exacerbated in IFN-γ or IFN-γ receptor deficient mice due to the ability of IFN-γ to

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... suppress IL-17 secretion. However, in proteoglycan-induced arthritis (PGIA), severe arthritis is dependent on the production of IFN-γ. We were therefore interested in determining the role of IL-17 in PGIA. We assessed the progression of arthritis in IL-17-deficient (IL-17 −/− ) mice and found the onset and severity of arthritis equivalent in wildtype (WT) and IL-17 −/− mice. Despite evidence that IL-17 is involved in neutrophil recruitment, synovial fluid from arthritic joints showed a comparable proportion of Gr1 + neutrophils in WT and IL-17 −/− mice. IL-17 is also implicated in bone destruction in autoimmune arthritis, however histological analysis of the arthritic joints from WT and IL-17 −/− mice revealed a similar extent of joint cellularity, cartilage destruction and bone erosion despite significantly reduced RANKL expression. There were only subtle differences between WT and IL-17 −/− in pro-inflammatory cytokine expression, T cell proliferation and autoanibody production. These data demonstrate that IL-17 is not absolutely required for autoimmune arthritis and production of other proinflammatory mediators are sufficient to compensate for the loss of IL-17 in PGIA.