We had hypothesized that glomerular damage would activate glomerular cells to induce and secrete mature IL-1b and IL-18 by activating the NLRP3-ASC-caspase-1 axis, a hypothesis not supported by our results. In contrary, our data show that intrinsic glomerular inflammation develops independent of the NLRP3-ASC-caspase-1 axis, possibly due to an inability for intrinsic glomerular cells to induce pro-IL-1b and to activate caspase-1 via NLRP3. The redundant role of NLRP3, ASC, and caspase-1 in antiserum induced glomerular pathology was unexpected because previous studies had documented a non-redundant role of the NLRP3 inflammasome in two models of renal inflammation. Iver, et al. reported that Nlrp3-deficient mice are partially protected from intrarenal cytokine signaling, neutrophil recruitment, and renal failure associated with postischemic tubular necrosis . Vilaysane, et al. induced GSK1363089 c-Met inhibitor tubulointerstitial inflammation by UUO in Nlrp3-deficient mice and found less tubular damage and interstitial fibrosis as compared to wildtype mice . The latter study addressed the contribution of NLRP3 activation in intrinsic renal cells by experiments with bone marrow chimeric mice and found that NLRP3 is required in both immune cells and nonimmune cells for the development of tubular damage and interstitial fibrosis of the same extent as in wildtype mice . Our current study excludes a similar role of NLRP3 in the glomerular compartment. LPS/ATP was unable to elicit caspase-1 activation and IL-1b release in freshly isolated glomeruli, in mesangial cells, glomerular endothelial cells, or podocytes while the same conditions were sufficient to induce IL-1b release in renal dendritic cells. Isolated AB1010 glomeruli and tubulointerstitial fractions form anti-GBM injected mouse supported our finding that IL-1 beta processing in confined to the extra glomerular compartment. Our data extend on a previous report by Timoshanko, et al. that concluded from bone marrow chimera experiments with Il-1bdeficient mice that only leukocyte-derived IL-1b contributes to autologous anti-GBM nephritis . Altogether, these observations have two implications: first, intrinsic glomerular cells cannot secrete IL-1b because they neither induce pro-IL-1b nor do they activate the NLRP3-ASC-caspase-1 axis; second, normal glomeruli harbour negligible numbers of dendritic cells which is consistent with lineage tracking studies of the mouse kidney and with immunohistochemical studies of the human kidney .