Figure 6

MFG-E8 effects autoantibody production and immune complex deposition. (a) Splenomegaly was visualized in the spleens from pristane-treated Mfge8^−/− mice, and spleen/weight ratios in mice with pristane-induced lupus were calculated (n=8–12 mice per group). (b) Histopathology of the spleens from pristane-treated Mfge8^−/− and WT mice; Fo= B-cell follicle. White arrows indicated infiltrated oil droplets or megakaryocytes. (c) The serum ANA titers from Mfge8^−/− and WT mice with pristane exposure for 24 weeks were detected by immunofluorescence (n=8–12 mice per group). (d) The serum anti-dsDNA antibody titers and ANCA in the Mfge8^−/− and WT mice after a 24-week pristane exposure were determined by immunofluorescence (n=8–12 mice per group); the proportion of c-ANCA and p-ANCA was calculated. (e) Left, with Masson-trichrome staining, histopathology of the lungs from Mfge8^−/− and WT mice after exposure to pristane for 24 weeks were shown; right, deposition of C3 (green) and IgG (red) in the lungs from Mfge8^−/− and WT mice were displayed. (f) Left, the histopathology of renal tissues from the Mfge8^−/− and WT mice exposed to pristane for 24 weeks were shown with PAS staining; right, deposition of C3 (green) and IgG (red) in glomeuli of kidney tissues from the Mfge8^−/− and WT mice were shown. (g) Composite scores of C3 and IgG were averaged and shown. (h) Left, albuminuria and creatinine in urine were detected by ELISA (n=8–12 mice per group), and albuminuria-to-creatinine ratios were calculated; right, the Kim-1 levels in urine were examined with ELISA (n=8–12 mice per group). For all experiments, data are shown as means±S.E.M., *P<0.05, **P<0.01; ns, not significant