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. Author manuscript; available in PMC: 2017 Feb 15.
Published in final edited form as: J Immunol. 2016 Jan 15;196(4):1495–1506. doi: 10.4049/jimmunol.1403251

Figure 5. Cell-autonomous and systemic augmentation of NRD1, characteristic for diabetes-prone NOD mice, determines defective VTCN1 presentation in multiple cell types.

Figure 5

(A) Representative images (left) and quantitative analysis (right) of pancreatic cryosections from NOD and B6g7 chimeric mice collected 10 weeks after the bone marrow transfer (n=3-4 mice/group). Scale bars, 50 μm. (B) Representative images (left) and quantitative analysis (right) of peritoneal MФs isolated from NOD and B6g7 chimeric mice; Scale bars, 10 μm. A, B Red dots and the horizontal lines in each box indicate the mean and the median values, respectively. (C) RT-qPCR analysis of VTCN1 (left) and NRD1 (right) mRNAs in peritoneal MФs isolated from NOD and B6g7 chimeric mice. The generated chimeras were: NOD-EGFP→NOD (NOD-EGFP donor into NOD recipient), B6g7→NOD-EGFP (B6g7 donor into NOD-EGFP recipient), NOD-EGFP→B6g7 (NOD-EGFP donor into B6g7 recipient) and B6g7→B6g7 (B6g7 donor into B6g7 recipient); *p<0.05; **p<0.01; ***p<0.001.