In lupus nephritis, dysregulated cytokines create a “cytokine storm” where IL-18—significantly elevated in serum (especially during active nephritis) and overexpressed in renal tubulointerstitium (correlating with inflammatory infiltration)—acts as a central hub by synergizing with IFN-γ, IL-1β, IL-12, IL-23, and BAFF to drive renal injury: promoting IFN-γ/Th1 responses with IL-12 (12), amplifying NLRP3 inflammasome cascades with IL-1β (39), enhancing Th17-mediated neutrophil recruitment (40), and forming a BAFF-driven autoreactive B-cell loop (41). Here, NLRP3 is linked to nephritis.