Furthermore, in a cellular model of IgA nephropathy established by culturing human renal tubular epithelial cells (HK-2 cells) with conditioned medium from IgA-stimulated human mesangial cells (HMCs), NLRP3 mRNA and protein expressions were significantly upregulated in HK-2 cells, accompanied by increased levels of ASC and caspase-1-indicating that mesangial-derived inflammatory signals can propagate NLRP3 activation to tubular compartments, thereby linking glomerular injury to tubulointerstitial inflammation (168). This evidence concerns the gene NLRP3 and IgA glomerulonephritis.