Abstract
Mouse models of inflammatory arthritis are strongly driven by excessive production of interleukin (IL)-1β. Much attention has focused on the generation of IL-1β by inflammasomes and caspase 1 in monocytes and macrophages. However, a number of other proteases can also process pro-IL-1β into the mature, bioactive cytokine. Despite that arthritis has complex etiologies based on genetic and environmental factors, global blockage of IL-1β signaling strongly ameliorates experimental models of arthritis. Yet, the relative contribution of the different IL-1β processing enzymes to disease initiation and perpetuation is elusive. Two papers in this issue of Arthritis & Rheumatism by Joosten et al. and Guma et al. shed more light on the complex proteolytic mechanisms behind excessive IL-1β maturation and release that perpetuates experimental models of inflammatory arthritis, which will have significant implications for designing future treatment strategies.
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