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. 1997 Oct 6;186(7):989–997. doi: 10.1084/jem.186.7.989

Figure 2.

Figure 2

Figure 2

Figure 2

Histological analysis of pancreatic islets. (A) Comparable degree of insulitis in pancreata of perforin-competent (+/0, top) and perforin-deficient (0/0, bottom) NOD mice. Pancreas sections from young (8-wk-old) and adult (55-wk-old) mice were stained with either hematoxylin and eosin (HE) or used for immunohistochemistry with CD4- or CD8-specific antibodies. Antibody binding resulted in red staining. (B) Presence of insulin-containing β cells in the islets of diabetic perforin-deficient mice. Sections from a 30-wk-old heterozygous and a 41-wk-old perforin-deficient diabetic NOD mouse were stained either with hematoxylin and eosin (HE) or with insulin-specific antibodies (red staining). Arrowheads in the left panel indicate reddish, eosinophilic dying islet cells. (C) Pancreatic islets of diabetic heterozygous and perforin-deficient NOD mice (both 7–10 wk old) after injection with cyclophosphamide. Diabetes occurred in the heterozygous mice 13 d after the first injection with 6 mg cyclophosphamide and in the perforin-deficient mouse 16 d after the second injection. Pancreas sections were either stained with hematoxylin and eosin (HE) or antiinsulin antibodies (red staining). Note the presence of insulin-containing β cells in the diabetic perforin-deficient NOD mouse and their lower intensity of insulin staining compared to islets from a healthy, untreated control C57BL/6 mouse.