Fig. 5

Anti-CEACAM1 mAb treatment enhances CD8⁺ T cell expansion and viral control. a Experimental setup. b, c. One group of wild-type (WT) and Ceacam1^–/– mice received anti-CEACAM1 mAb, and another group received an equal amount of isotype antibody on day –1 and day 3, followed by infection with 2 × 10⁴ PFU of LCMV-Docile on day 0. b, c Graphs showing percentage of virus-specific Tet-GP33⁺ CD8⁺ T cells in blood (b) and viral titers in serum (c) in indicated groups over the indicated times. Statistical significance is shown between the WT + IgG-treated groups and the WT + α-CC1 mAb-treated groups (n = 3–6 per group). d Experimental setup. e Wild-type (WT) mice were infected with 2 × 10⁶ PFU of LCMV-Docile on day 0. On day 16 after infection, mice were treated with 200 µg anti-CEACAM1 mAb per mouse or with an isotype antibody. e Viral titers in serum (left panel) over the indicated times and in indicated organs (right panel) on day 60 after infection (n = 4–8 per group). f Experimental setup. g–i Ceacam1^–/– mice were given 1 × 10⁴ P14 × CD45.1 WT splenocytes on day –2. One group of these mice was additionally treated with anti-CEACAM1 mAb, and another group was treated with an equal amount of an isotype antibody on day –1 and on day 3, followed by infection with 2 × 10⁴ PFU of LCMV-Docile on day 0. Mice were analyzed on day 8 after infection. g Absolute number of transferred Tet-GP33⁺ CD45.1⁺ CD8⁺ T cells in blood and spleen of host Ceacam1^–/– (CD45.2) mice (n = 5–7 per group). h Intracellular cytokine IFN-γ secretion from transferred P14 × CD45.1 WT CD8⁺ T cells (n = 5–7 per group). i Viral titers in the indicated organs of the recipient mice (n = 5–7 per group). *P < 0.05, **P < 0.01, ***P < 0.001 (Student’s t test). ns = not significant. Data are representative of two (b, c, e, g–i) independent experiments (mean ± SEM; b, c, e, g–i)