Skip to main content
. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Nat Immunol. 2009 Sep 27;10(11):1185–1192. doi: 10.1038/ni.1790

Figure 1. Antigen-specific tolerance blocks diabetes, TCR signaling and Ca++ flux in a PD-L1-dependent manner.

Figure 1

(a) p31-SP tolerance prevents T1D induced by BDC2.5 T cell adoptive transfer. Activated BDC2.5 T cells were transferred to NOD mice followed with p31-SP (p31 Tolerized) or SHAM-SP (Activated control) treatment the same day. The percentages of diabetic mice receiving SHAM-SP (n=8) compared to p31-SP protected mice are shown (n=8). (b) p31-SP tolerized cells have decreased ability to flux calcium upon TCR ligation. BDC2.5 TCR CD4+ T cells treated in vivo with p31-SP (p31-Tolerized) or SHAM-SP (Control) were purified and loaded with Indo-1. Cells were activated with anti-CD3 (5μg/ml) and cross-linking antibody or ionomycin as indicated, and calcium flux was measured. (c) PD-L1 blockade breaks tolerance. 2×106 p31-SP tolerized BDC2.5 TCR transgenic T cells were transferred to naïve recipients followed by anti-PD-L1, anti-CTLA-4 or isotype control antibody treatments. Recipient mice were monitored for the development of T1D by blood glucose measurements. The percentage of diabetic mice receiving anti-PD-L1 (n=5), isotype control (n=5) and anti-CTLA-4 (n=5) are shown. Data are representative of three or more independent experiments except (c) which was from two independent experiments.