IL1B and arthritic joint disease: The mechanisms underlying these in vivo phenomena became more clear since it has been described IL-1RI expression first on IL-17+CD4+ T cells of SKG mice (that spontaneously develop arthritis) (40), and later on, by the demonstration that IL-1 signaling is required for the upregulation of IRF4 and RORC (two fundamental Th17 transcription factors) during the early Th17 lineage programing and to sustain its differentiation (41).