Fig. 1
Mitochondrial autoantigen-based pMHCII-NPs expand cognate TR1 cells. a Percentages of tetramer+ CD4+ cells in blood of NOD vs. NOD.c3c4 mice vs. age (4 and 5 mice/strain, respectively). b Percentage of tetramer+ CD4+ cells in blood of pMHCII-NP-treated NOD.c3c4 vs. untreated or control NP-treated NOD or NOD.c3c4 mice. Data correspond to: 2–5 untreated NOD mice (1 experiment); 2–5 untreated and 15 Cys-NP-treated NOD.c3c4 mice and 18 PDC166–181/IAg7-NP-treated NOD.c3c4 mice (5 experiments); three untreated and five PDC82–96/IAg7-NP-treated NOD.c3c4 mice (2 experiments); and 3–5 untreated and 3–5 BDC2.5mi/IAg7-NP-treated NOD.c3c4 mice (2 experiments). c Percentages of tetramer+CD4+ cells in various organs from the mice in (c) at the end of therapy. d Percentages of tetramer+CD4+ cells in lymphoid organs and liver of NOD.c3c4 mice treated for 9 weeks with PDC82–96/IAg7-NPs or PDC166–181/IAg7-NPs. Data correspond to four untreated and three PDC166–181/IAg7-NP treated, and six untreated and eight PDC82–96/IAg7-NP-treated NOD.c3c4 mice. e Percentages of tetramer+CD4+ cells in liver and various lymphoid organs in the NOD.c3c4 mice treated with BDC2.5mi/IAg7-NPs from panel b. f Expression of TR1 markers by PCLN tetramer+CD4+ cells. g Cytokine profile of sorted splenic tetramer+CD4+ and tetramer–CD4+ cells upon stimulation with peptide-pulsed DCs. Data correspond to four PDC166–181/IAg7-NP-treated NOD.c3c4 mice from three experiments. Data are represented as mean ± SEM. P values were calculated via two-way ANOVA (a and b) or Mann–Whitney U (c–e)
