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 4
In RIP-LCMV mice, apoptosis of autoaggressive (LCMV-specific) CD8 lymphocytes in the PDLN is enhanced after protective viral infection. (a) Frequency of LCMV-NP–specific pCTLs in RIP-LCMV-NP mice after secondary i.p. infection with 10⁵ PFUs of LCMV-Arm or LCMV-Past administered 4 weeks after initial LCMV-Arm infection. Note that the reduced pCTL frequency in the PDLN after secondary infection with LCMV-Past correlated with the drastically lower incidence of diabetes in those mice. *pCTL frequencies in the spleen at day 3 after primary i.p. infection with 10⁵ PFUs of LCMV-Arm or LCMV-Past are displayed as a reference. nd, not determined. (b) RIP-LCMV-NP mice were infected i.p. with 10⁵ PFUs of LCMV-Arm and, after 1 month, with 10⁵ PFUs of either LCMV-Arm or LCMV-Past. At day 3 after secondary infection, PDLN CD8 lymphocytes were stained with anti-CD8 mAb, H-2D^b(GP₃₃)- or H-2D^b(NP₃₉₆)-tetramers, and annexin V. CD8^hi, H-2D^b-tetramer^hi cells (left panels, dot blots) were analyzed with annexin V for apoptosis (right panels, histograms). The relative numbers of CD8^hi, H-2D^b-tetramer^hi cells and annexin V^hi cells are indicated as percentage of gated cells.