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. 2016 Mar 28;27(12):3666–3677. doi: 10.1681/ASN.2015101077

Figure 3.

Figure 3.

IL-17F neutralization attenuates crescentic GN. (A) Representative photographs of PAS-stained kidney sections from control mice, wild-type mice treated with isotype antibody (250 μg intraperitoneal injection on day 0 and day 4 of NTN), and wild-type mice treated with anti–IL-17F antibody (250 μg intraperitoneal injection on day 0 and day 4 of NTN), at day 8 of NTN (original magnification ×400). (B) Quantification of glomerular crescent formation, interstitial area, and glomerular sclerosis of controls (n=3), wild-type mice treated with isotype antibody (n=9), and wild-type mice treated with anti–IL-17F antibody (n=9) 8 days after induction of nephritis. (C) BUN levels, serum creatinine, and ACR of the aforementioned groups 8 days after induction of nephritis. (D) Quantification of tubulointerstitial GR-1+ cells, tubulointerstitial F4/80+ cells, and glomerular MAC-2+ cells of the aforementioned groups 8 days after induction of nephritis. (E) Quantification of tubulointerstitial CD3+ T cells and glomerular CD3+ T cells of the aforementioned groups 8 days after induction of nephritis. (F) Real-time RT-PCR analyses of renal mRNA expression of different chemokines in the aforementioned groups. mRNA levels are expressed as x-fold of controls. Symbols represent individual data points with the mean as horizontal line, or bar graphs with the mean±SD. *P<0.05; **P<0.01.