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. 2004 Nov 1;114(9):1290–1298. doi: 10.1172/JCI22557

Figure 1.

Figure 1

Molecular mimicry can accelerate but not easily initiate autoimmune diabetes. (A) Molecular mimicry is insufficient to prime naive autoreactive CD8 T cells and cause autoimmune diabetes. RIP-LCMV-NP mice were infected with 105 PFU LCMV-Arm (open circles), LCMV-Arm-Var (filled triangles), or PV alone (filled circles). (B) Primed autoreactive cells can become activated via molecular mimicry and accelerate disease. RIP-LCMV-NP mice were infected with either 105 PFU LCMV-Arm (open circles, filled circles) or 105 PFU PV (open triangles, filled triangles) on day 0 and, as indicated, received a secondary inoculation (2nd inf.) with PV (open triangles, filled circles) 28 days after the priming LCMV infection. As a comparison, the incidence data to RIP-LCMV-NP mice infected with LCMV alone are displayed (open circles). For both studies, blood glucose values were determined at weekly intervals. Mice with blood glucose levels above 300 mg/dl were considered diabetic. It is evident from these studies that secondary infection but not primary infection with PV can accelerate T1D development. Statistical analysis was done using the log rank test. Note that the diabetes onset curves for the groups LCMV alone versus LCMV-PV are significantly different (P = 0.0066).