X-axis, and the expression level of each TLR relative to expression is shown β-actin along the Y-axis. Only was significantly correlated with the severity of TII. TLR4 Figure 6. Relationship between the inflammasome and TII in ANCAGN. (A) The expression levels of and relative to expression are represented along TLR4 IL-1β β-actin the X- and Y-axis, respectively. (B) The severity grade of TII is shown along the and the expression level of relative to expression is shown along NLRP3 β-actin the Y-axis. (C) Expression levels of and relative to expression NLRP3 caspase1 β-actin are represented along the X- and Y-axis, respectively. Figure 7. Representative immunohistochemistry results for the role of the inflammasome in ANCAGN. (A) TLR4-positive cells were detected in the tubulointerstitium, and not in the glomerulus. Magnification, 400, boxed area 1,000. (B) NLRP3: Magnification, 100, boxed area 800. (C) caspase1: Magnification, 100, boxed area, 1,000. References 1. Jennete JC TD. Pauci-immune and antineutrophil cytoplasmic autoantibody-mediated crescentic glomwrulonephritis and vasculitis. Philadelphia: Lippincott Williams & Wilkins; 2007. 2. Seshan SV DAV, Appel GA, Churg J. Renal vasculitis: cllasiffication and atlas of tubulointerstitial and vascular diseases. Baltimore: Williams & Wilkins; 1999. 3. Clarke BE, Ham KN, Tange JD, Ryan GB. Origin of glomerular crescents in rabbit nephrotoxic nephritis. J Pathol. 4. Silva FG, Hoyer JR, Pirani CL. Sequential studies of glomerular crescent formation in rats with antiglomerular basement glomerulonephritis and the role of coagulation factors. Lab
X-axis, and the expression level of each TLR relative to β-actin expression is shown along the Y-axis. Only TLR4 was significantly correlated with the severity of TII. Figure 6. Relationship between the inflammasome and TII in ANCAGN. (A) The expression levels of TLR4 and IL-1β relative to β-actin expression are represented along the X- and Y-axis, respectively. (B) The severity grade of TII is shown along the and the expression level of NLRP3 relative to β-actin expression is shown along the Y-axis. (C) Expression levels of NLRP3 and caspase1 relative to β-actin expression are represented along the X- and Y-axis, respectively. Figure 7. Representative immunohistochemistry results for the role of the inflammasome in ANCAGN. (A) TLR4-positive cells were detected in the tubulointerstitium, and not in the glomerulus. Magnification, 400, boxed area 1,000. (B) NLRP3: Magnification, 100, boxed area 800. (C) caspase1: Magnification, 100, boxed area, 1,000. References 1. Jennete JC TD. Pauci-immune and antineutrophil cytoplasmic autoantibody-mediated crescentic glomwrulonephritis and vasculitis. Philadelphia: Lippincott Williams & Wilkins; 2007. 2. Seshan SV DAV, Appel GA, Churg J. Renal vasculitis: cllasiffication and atlas of tubulointerstitial and vascular diseases. Baltimore: Williams & Wilkins; 1999. 3. Clarke BE, Ham KN, Tange JD, Ryan GB. Origin of glomerular crescents in rabbit nephrotoxic nephritis. J Pathol. 4. Silva FG, Hoyer JR, Pirani CL. Sequential studies of glomerular crescent formation in rats with antiglomerular basement glomerulonephritis and the role of coagulation factors. Lab
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