Cure of prediabetic mice by viral infections involves lymphocyte recruitment along an IP-10 gradient
J. Clin. Invest. Urs Christen, et al. 113:74 doi:10.1172/JCI17005 [Go to this article.]

Figure 1
Prevention of T1D in NOD and RIP-LCMV mice by LCMV infection given during the prediabetic phase. (a) Cumulative incidence of diabetes in RIP-LCMV-NP mice infected i.p. with 10⁵ PFUs of LCMV-Arm on day 0. One month after infection, mice were infected i.p. with 10⁵ PFUs of either LCMV-Arm (Arm-Arm) or LCMV-Past (Arm-Past). Blood glucose was measured in biweekly intervals for at least 9 months, and values greater than 300 mg/dl were considered diabetic. The number of diabetic mice and the total number of animals used per group are indicated in brackets. (b) Groups of 10–15 RIP-LCMV-NP H-2^b mice were infected i.p. with 10⁵ PFUs of various LCMV strains (single infection). Blood glucose values were determined as described in Methods. The NP escape variant contains a single amino acid change from F to L in position AA404 of the immunodominant H-2D^b NP₃₉₆ peptide, which prevents binding of the variant NP₃₉₆ to H-2D^b (36). pCTL analysis was performed 7 days after infection as described in Methods. Note that RIP-NP mice express the LCMV-NP antigen in their thymus in addition to their islets and therefore have reduced numbers of NP CTLs in their periphery and develop diabetes more slowly, as reported by us previously (24). Non-Tg, nontransgenic C57BL/6 mice. (c) Groups of 10–15 NOD mice were infected i.p. with 10⁵ PFUs of LCMV-Arm (single infection) at week 10 or 20 of age. Blood glucose values were determined every 4 weeks.