Figure 1
Figure 1. Deficiencies of B7-H1 and B7-DC abrogate oral tolerance. Wild-type (WT) mice (A-B), Cd80/Cd86−/− mice (C-D), B7h1−/− mice (E-F), B7dc−/− mice (G-H), and B7h2−/− mice (I-J; 5 per group) were fed PBS (none) or OVA protein, and then systemically immunized with OVA protein 7 days after the oral priming. Subsequently, serum and Sp CD4+ T cells were collected from each group of mice 14 days after systemic immunization. (A,C,E,G,I) Serum OVA-specific IgG1 production was measured by ELISA. (B,D,F,H,J) Proliferative response of Sp CD4+ T cells to WT Sp CD11c+ DCs in the presence or absence of OVA protein was measured by [3H]thymidine incorporation. *P < .01 compared with nonfed mice. Data are the mean ± SD, and the results are representative of 4 independent experiments.

Deficiencies of B7-H1 and B7-DC abrogate oral tolerance. Wild-type (WT) mice (A-B), Cd80/Cd86−/− mice (C-D), B7h1−/− mice (E-F), B7dc−/− mice (G-H), and B7h2−/− mice (I-J; 5 per group) were fed PBS (none) or OVA protein, and then systemically immunized with OVA protein 7 days after the oral priming. Subsequently, serum and Sp CD4+ T cells were collected from each group of mice 14 days after systemic immunization. (A,C,E,G,I) Serum OVA-specific IgG1 production was measured by ELISA. (B,D,F,H,J) Proliferative response of Sp CD4+ T cells to WT Sp CD11c+ DCs in the presence or absence of OVA protein was measured by [3H]thymidine incorporation. *P < .01 compared with nonfed mice. Data are the mean ± SD, and the results are representative of 4 independent experiments.

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