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Members of the Toll-like receptor (TLR) family serve as pathogen sensors and participate in local autoimmune responses. This study found a correlation between glomerular injury and TLR expression by analysing BXSB/MpJ- Yaa  (BXSB- Yaa ) lupus model mice. In isolated glomeruli, the mRNA expression of several TLRs was higher in BXSB- Yaa  mice than in healthy control BXSB mice. In particular, the expression of  Tlr8  and its downstream cytokines was markedly increased. In mouse kidneys, TLR8 protein and mRNA localized to podocytes, and TLR8 protein expression in the glomerulus was higher in BXSB- Yaa  mice than in BXSB mice. In BXSB- Yaa  mice, the glomerular levels of  Tlr8  mRNA negatively correlated with the glomerular levels of podocyte functional markers ( Nphs1, Nphs2,  and  Synpo ) and positively correlated with urinary albumin levels. Furthermore, the glomerular and serum levels of miR-21, a putative microRNA ligand of TLR8, were higher in BXSB- Yaa  mice than in BXSB mice. The urinary levels of  Tlr8  mRNA were also higher in BXSB- Yaa  mice than in BXSB mice. In conclusion, the overexpression of TLR8 correlates with the progression of podocyte injury in glomerulonephritis. Thus, altered levels of urinary  Tlr8  mRNA might reflect podocyte injury.

Overexpression of Toll-like receptor 8 correlates with the progression of podocyte injury in murine autoimmune glomerulonephritis