While caspase-1 inhibition affects both biologically active IL-18 and IL-1β, our data align with prior clinical studies establishing IL-18 as the principal driver of LN.6, 8 The weak correlation between IL-1β and SLE activity in humans,9 as well as the failure of IL-1 receptor antagonism to ameliorate LN in our model, reinforces the concept that IL-18, more than IL-1β, mediates LN as a central interleukin in SLE. Here, IL1B is linked to systemic lupus erythematosus.