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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: J Autoimmun. 2015 Apr 2;59:8–18. doi: 10.1016/j.jaut.2015.01.003

Fig. 2.

Fig. 2

Assessment of renal disease in groups of WKY rats (n=6) immunized with sense pCol(24–38) peptide, and anti-sense peptides c-α3-Gly and c-α3-Arg. Results shown represent individual animals in each group at week six after immunization for pCol(24–38) and week eight after immunization for c-α3-Gly and c-α3-Arg. (A) Urine analysis for albumin excretion (*p<0.001; pCol(24–38) versus c-α3-Arg, **p<0.05; c-α3-Gly versus c-α3-Arg). (B) Glomerular abnormalities graded as severe (extensive segmental necrosis/crescent formation), abnormal (segmental necrosis and/or extracapillary proliferation), or normal (*p<0.001; pCol(24–38) versus c-α3-Arg, **p<0.01; c-α3-Gly versus c- α3-Arg). (C–E) Light microscopy of kidney tissue showing: (C) marked segmental fibrinoid necrosis of the glomerular tuft with crescent formation at week 6 from an animal immunized with pCol(24–38); (D) severe crescentic glomerulonephritis with fibrinoid necrosis at week 8 from an animal immunized with c-α-3-Gly; and (E) normal glomerular architecture from an animal immunized with c-α3-Arg. (F–H) Direct immunofluorescence of kidney tissue showing: (F) strong linear deposits of IgG along the GBM at week 6 from an animal immunized with pCol(24–38), (G) weak, intermittent deposits of IgG at week 8 from an animal immunized with c-α3-GLY and (H) background fluorescence from an animal immunized with c-α3-Arg. Magnification ×300.