Fig. 3. Intestinal OVA-specific CTLs cannot be induced in CD11c⁺ DC-depleted mice.

a CD11c-DTR Tg mice and non-Tg littermates were i.p. injected with 4 ng of DT/g of body weight. One day later, MLN cells and SP cells were isolated from the mice, double-stained with FITC-labeled anti-CD11c Ab and PE-labeled anti-CD8, anti-DEC-205, or anti-DCIR2 Ab, and analyzed by flow cytometry. b, c CD11c-DTR Tg mice and non-Tg littermates were i.p. injected with PBS or DT on days 0 and 5, and orally administered 100 mg of OVA alone or plus 10 μg of CTA subunit, CTB subunit, or CT on days 1 and 6. IELs were isolated from the mice 2 days after the second oral administration, double-stained with PE-labeled H-2K^b/OVA tetramer-SIINFEKL and APC-labeled anti-CD8β Ab, and analyzed by flow cytometry (b). OVA-specific CTL responses of the IELs as described in (b) were measured by the ⁵¹Cr-release assay using EL4 cells pulsed with 4 μM OVA-peptide SIINFEKL and E.G7-OVA cells as target cells (c). The effector:target (E:T) ratio was 50:1. Data are shown as the mean + SE in triplicate. The results are representative of two independent experiments