TLR2 can recognize acylated bacterial lipopeptides and trigger the secretion of mature IL-1β. In Immunity, Stehlik and colleagues identify NLRP7 as an intracellular sensor of bacterial lipopeptides. Infection with mycoplasma or exposure to acylated lipopeptides triggers the aggregation of ASC, NLRP7 and pro-caspase-1 in inflammasome complexes in human macrophages. Knockdown of either TLR2 or NLRP7 results in less inflammasome activation and secretion of IL-1β and IL-18 in response to acylated lipopeptides, but knockdown of other NLR proteins does not. Neither scavengers of reactive oxygen species (ROS) nor a high potassium concentration, which blunt mitochondrial stress-mediated inflammasome activation, result(s) in less NLRP7 inflammasome activity. These findings suggest that activation of the NLRP7 inflammasome in response to acylated lipopeptides differs from the activation of those containing NLRP3.

Immunity (16 February 2012) doi:10.1016/j.immuni.2012.01.009