NLRP10 is a cytosolic inflammasome sensor protein that functions as a pattern recognition receptor in innate immunity. As a member of the NLR family lacking a canonical leucine-rich repeat domain 1, NLRP10 assembles ASC-dependent inflammasome complexes that detect mitochondrial damage in an mtDNA-independent manner 2, triggering caspase-1-dependent secretion of pro-inflammatory cytokines IL-1β and IL-18 1. NLRP10 exerts dual roles: it inhibits caspase-1 autoprocessing and PYCARD-mediated apoptosis while simultaneously promoting inflammasome activation under stress conditions 3. In epithelial cells, particularly keratinocytes and intestinal epithelial cells, NLRP10 protects against autoinflammation and maintains barrier homeostasis 14. In skin, NLRP10 promotes keratinocyte survival by preventing caspase-8 recruitment to the death-inducing signaling complex and stabilizes p63 to drive differentiation and barrier function 4. NLRP10 downregulation associates with atopic dermatitis susceptibility 4. In periodontal disease, NLRP10 regulates IL-1α production via ERK activation 5 and can promote NLRP1/NLRP3 inflammasome activation through ROS/MAPK/NF-κB signaling under AGE stimulation 6. These findings suggest NLRP10 represents a therapeutic target for inflammatory and autoimmune diseases.