The previously established hypersensitivity of the Nlrp3R258W mice was tested by delayed-type hypersensitivity (DTH) induction with DNCB28. The hyperkeratosis and a neutrophil infiltrate, with the related MPO release, that is induced in the skin of Nlrp3R258W mice with this treatment was significantly attenuated by ablating Zbtb16 (Fig. 3c, d). The fact that ablating Zbtb16 ameliorates the effects of a hyperactive Nlrp3 mutant demonstrates the impact of ZBTB16 on inflammasome activity. The effectiveness of ZBTB16 to moderate inflammation in the face of constitutive NLRP3 activity also suggests that ZBTB16 functions downstream of the inflammasome sensor proteins.
