Developmental control of CD8⁺ T cell–avidity maturation in autoimmune diabetes
J. Clin. Invest. Bingye Han, et al. 115:1879 doi:10.1172/JCI24219 [Go to this article.]

Figure 3
Avidity and diabetogenic potential of peripheral IGRP_206–214 tetramer⁺ cells from 17.6α/8.3β-Tg versus 17.4α/8.3β-Tg animals. (A) Tetramer-binding ability of 17.6α/8.3β versus 17.4α/8.3β CTL lines (generated by stimulation of naive splenic CD8⁺ cells with NRP-V7 in the presence of rIL-2). (B) Cytolytic activity of in vitro–differentiated CTL lines against NRP-V7 peptide-pulsed RMA-S/K^d targets (percentages of 51-Cr release against targets pulsed with the negative control peptide TUM were subtracted). Since Tg CD8⁺ T cells from both types of mice do not expand (or survive) when stimulated with irrelevant peptides, these assays reflect differences in cytolytic activity between CD8⁺ cells of identical antigenic specificity but different avidity. (C) Secretion of IFN-γ by purified CD8⁺ splenocytes (adjusted for the number of IGRP_206–214 tetramer–positive cells) to various concentrations of NRP-V7 (donor mice were > 6 weeks old). (D) Cumulative incidence of diabetes in 8 (17.6α/8.3β-Tg) versus 214 (17.4α/8.3β-Tg) female mice for the period of time the former were followed.