TLR2 and IgA glomerulonephritis: Our results demonstrate that TLR2 and its main stress ligands are markedly upregulated in the kidney after UUO-injury, obstructive hydronephrosis (TLR2) and IgA nephropathy (TLR2) and identify TLR2 as an initiator of renal inflammation (neutrophil influx, cytokine induction) during progressive renal injury.