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Release b and IL-1 Links Complement-Mediated Inflammation Cutting Edge: The NLRP3 Inflammasome

The complement system is a potent component of the innate immune response, promoting inﬂammation and orchestrating defense against pathogens. However, dys-regulation of complement is critical to several autoimmune and inﬂammatory syndromes. Elevated expression of the proinﬂammatory cytokine IL-1 b is often linked to such diseases. In this study, we reveal the mechanistic link between complement and IL-1 b secretion using murine dendritic cells. IL-1 b secretion occurs following intracellular caspase-1 activation by inﬂammasomes. We show that complement elicits secretion of both IL-1 b and IL-18 in vitro and in vivo via the NLRP3 inﬂammasome. This effect depends on the inﬂammasome components NLRP3 and ASC, as well as caspase-1 ac-tivity. Interestingly, sublethal complement membrane attack complex formation, but not the anaphylatoxins C3a and C5a, activated the NLRP3 inﬂammasome in vivo. These ﬁndings provide insight into the molecular processes underlying complement-mediated inﬂammation and highlight the possibility of targeting IL-1 b to control complement-induced disease and pathologi-cal inﬂammation. The Journal of Immunology , 2013, 191: 000–000.