We next examined the response of BMDMs isolated from WT or Zbtb16-/- mice to different inflammasome triggers. ELISA and an immunoblotting assay of BMDMs stimulated with MSU and a range of other NLRP3 activators confirmed the defect observed in vivo as reduced processing of pro-IL-1β, pro-IL-18 and pro-Caspase-1 in the Zbtb16-/- cells (Fig. 2a–d). Notably, the expression of NLRP3, ASC, GSDMD and pro-IL-1β as well as the NIMA-related kinase 7 (NEK7), which is essential for NLRP3 inflammasome activation24,25, were unaffected by Zbtb16 expression (Fig. 2c, d and Supplementary Fig. 2a, b).
