Innate and adaptive effects of inflammasomes on T cell responses

Inflammasomes are protein complexes that form in response to pathogen-derived or host-derived stress signals. Their activation leads to the production of inflammatory cytokines and promotes a pyrogenic cell death process. The massive release of inflammatory mediators that follows inflammasome activation is a key event in alarming innate immune cells. Growing evidence also highlights the role of inflammasome-dependent cytokines in shaping the adaptive immune response, as exemplified by the capacity of IL-1β to support Th17 responses, or by the finding that IL-18 evokes antigen-independent IFN-γ secretion by memory CD8+ T cells. A deeper understanding of these mechanisms and on how to manipulate this powerful inflammatory system therefore represents an important step forward in the development of improved vaccine strategies.

► Inflammasome activation leads to production of bioactive IL-1β and IL-18.
► IL-1β promotes Th17 differentiation, IL-18 supports IL-12-driven Th1 polarization.
► IL-18 drives non-cognate lymphocyte activation, thereby improving immunity.
► manipulation of inflammasome activity and substrates can ameliorate vaccine strategies.