il1 receptor antagonistdeficient mice develop autoimmune arthritis due to intrinsic activation of il17producing ccr2v6 t cells interleukin17 il17producing t 17 cells have been implicated in inflammatory diseases but the underlying pathogenic mechanisms remain unclear here we show that both cd4 and 17 cells are required for the development of autoimmune arthritis in il1 receptor antagonist il1radeficient mice specifically activated cd4 t cells direct tcell infiltration by inducing ccl2 expression in joints furthermore il17 reporter mice reveal that the v6 subset of ccr2 t cells preferentially produces il17 in inflamed joints importantly because il1ra normally suppresses il1r expression on t cells il1radeficient mice exhibit elevated il1r expression on v6 cells which play a critical role in inducing them to produce il17 our findings demonstrate a pathogenic mechanism in which adaptive and innate immunity induce an autoimmune disease in a coordinated manner