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. 2003 Jul 7;100(15):8874–8879. doi: 10.1073/pnas.1033098100

Fig. 3.

Fig. 3.

DCs from CD1d-deficient mice are functionally impaired. (A) GM-CSF-secreting B16 melanomas recruit myeloid-type DCs that express significantly less cell surface MHC class II. WT, CD1d-heterozygous, and CD1d-deficient C57BL/6 mice were inoculated with live, GM-CSF-secreting B16 cells, and the expression of MHC class II on splenic myeloid-type DCs was determined 14 days later (P < 0.01 comparing CD1d–/–, n = 11 vs. CD1d+/–, n = 6, or CD1d+/+, n = 11). (B) MLRs induced by DCs are impaired in CD1d-deficient mice. Splenic DCs were isolated from mice injected with live, GM-CSF-secreting tumor cells and used to stimulate in vitro MLRs with splenocytes from SJL, SWR, PL/J, P/J, C3H, and B10.BR donors. Shown is a representative example from one of four experiments with identical patterns for MLR responses. (C) Presentation of peptide antigen to either the I-Ab:Ea52–68-specific hybridoma 1H3.1 or TCR transfectant H30 (32, 33) by DCs isolated from CD1d-deficient mice is impaired when compared with DCs isolated from WT mice. The data presented are representative of three experiments.

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