FIG. 1.

iNKT-cell activation prevents diabetes development after CVB4 infection. A: Diabetes incidence of female NOD mice (10 weeks old) inoculated intraperitoneally with CVB4 1 × 10⁵ PFU/mouse or PBS and treated with αGalCer (αGC) or control vehicle (untreated n = 14, αGC n = 15, CVB4 n = 14, CVB4 + αGC n = 15). *P < 0.05; **P < 0.005 by log-rank test. Data represent two pooled independent experiments. B: Age of diabetes onset of NOD mice that became diabetic. *P < 0.05; ***P < 0.0005 by Mann-Whitney U test. C: Diabetes incidence of female Proins2^−/− mice inoculated intraperitoneally with CVB4 1 × 10⁵ PFU/mouse or PBS and treated with αGC or control vehicle at 5–6 weeks of age (untreated n = 44, αGC n = 10, CVB4 n = 36, CVB4 + αGC n = 17). **P < 0.005; ***P < 0.0005 by log-rank test. Data represent two to four pooled independent experiments. D: Age of diabetes onset of Proins2^−/− mice that became diabetic. ***P < 0.0005 by Mann-Whitney U test. E: Histological scoring of insulitis was performed on pancreatic sections of Proins2^−/− mice from days 7 to 10 postinfection and stained with hematoxylin-eosin (n = 6 mice/group). Grade 0, no infiltration; grade 1, peri-islet lymphocytic infiltration; grade 2, <50% islet lymphocytic infiltration, and grade 3, >50% islet lymphocytic infiltration. F: Pancreata were isolated from Proins2^−/− mice on different days postinfection and weighed, and viral titers were determined on HeLa cell monolayers with a plaque assay technique. Mean ± SD viremia titers are expressed as PFU per gram of pancreas (n = 6 mice/group for each day).