NOD-like receptors

Stehlik and colleagues show that NLRP11 is an essential component of the NLRP3 inflammasome in human macrophages.

This Review from Masters and colleagues highlights how damage to intracellular organelles is linked to activation of the innate immune system. The authors propose that a better appreciation of such organellar homeostasis could lead to the identification of novel innate immune pathways and have therapeutic implications.

Nlrp3 inflammasome activation requires Nek7 recruitment to drive ASC speck formation. Here the authors show how Nlrp3 phosphorylation events control this Nek7 recruitment.

Post-translational modifications are important regulators of NLRP3 inflammasome activity. Here the authors show that the E3 ligase TRIM28 can SUMOylate NLRP3, thereby limiting its proteasomal degradation and increasing NLRP3 inflammasome activity.