Fig. 2.

Leptin deficiency protects from pristane-induced lupus renal disease. Twenty-eight weeks after treatment with pristane or saline, kidneys from WT and ob/ob mice were explanted, and sections were stained with hematoxylin/eosin (H/E) (A–C) or by indirect immunofluorescence for anti-IgM (D–F), anti-IgG (G–I), or anti-complement factor C3 (J–L). Only pristane-treated WT mice developed diffuse proliferative glomerulonephritis (B), Ig (E and H), and complement deposition (K). Original magnification, 10×. Data were obtained from five to six fields from six mice per group.