FcγRIII targeting by IVIg and 2.4G2 F(ab′)2 reduces nonimmune inflammatory response in FcγRIIB−/− mice, but not in FcγRIII−/− mice. (A) FcγRIIB−/− or FcγRIII−/− Balb/c mice were injected intraperitonealy with 2.4G2 F(ab′)2 (100 μg/20 g; top panel) or IVIg (40 mg/20 g; bottom panels), or their controls rat IgG F(ab′)2 or BSA, respectively, as indicated. After 24 hours, mice were subjected to surgery for unilateral ureteral obstruction on their left side and 2.4G2 or IVIg or control treatments were continued at 48-hour intervals until day 8 when animals were killed and kidney sections were analyzed. Photographs show immunohistologic staining of CD11b-positive cells in obstructed left kidneys. Corresponding quantitative analysis of infiltrating cells of several animals (n = 6) is shown on the right. (*P < .05,**P < .01; nonparametric Mann-Whitney test). (B) Expression of MCP-1 and TNFα mRNA were analyzed by quantitative real-time PCR in obstructed kidney from mice treated with either IVIg or 2.4G2 F(ab′)2 (white bar) or with their control treatment BSA or rat IgG F(ab′)2 (black bar). Data represent relative mRNA expression levels of obstructed versus controlateral kidneys after normalization to GADPH (*P < .05; nonparametric Mann-Whitney test).
