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. Author manuscript; available in PMC: 2016 Jun 15.
Published in final edited form as: J Immunol. 2015 May 15;194(12):5713–5724. doi: 10.4049/jimmunol.1500277

Figure 1. Ido1 induction is a key feedback mechanism limiting anti-glomerular basement membrane antibody driven nephritis.

Figure 1

Mild nephrotoxic serum nephritis was induced in wild type and Ido1 KO mice by injection of low-dose NTS. (A) Functional status of kidney was assessed by albuminuria (albumin/creatinine ratio, ACR) and blood urea nitrogen (BUN) measurement in urine and blood samples. (B) Paraffin embedded kidney sections stained with periodic acid–Schiff reagent and hematoxylin. Images are representative of 5 mice per group. Bar= 100 μm. (C) Glomerular and tubular pathology of mice from A was scored in a blinded manner. For % of glomeruli with crescent determination at least 100 glomeruli were examined. (D) Survival of wild type and Ido1 KO mice challenged with low and high dose NTS. (E) Kidney cryosections from mice 5 days after low-dose NTS injection were stained for IDO1 (red) and the podocyte antigen synaptopodin (synp, green) or the endothelial antigen CD31 (green). Bar= 100 μm. (F) Ido1 mRNA from purified glomeruli was measured by rtPCR 5 days after low dose NTS injection from B6 mice with the genotypes indicated. For A, C, and F *=p<0.05 and **=p<0.01 as determined by student t test. For A, C, and F n=5 mice per group and the error bars indicate standard deviation (SD). For D, n=8 to 12 mice per group. Each experiment shown was repeated three times with similar results.