Restoration of the antibody response to IgE/antigen complexes in CD23-deficient mice by CD23(+) spleen or bone marrow cells

Mice immunized with IgE/Ag complexes produce significantly more Ag-specific Abs than mice immunized with Ag alone. The enhancement is mediated via the low-affinity receptor for IgE (Fc epsilon RII: or CD23), as shown by its c omplete absence in mice pretreated with mAbs specific for CD23 and in CD23- deficient mice. Because the constitutive expression of murine CD23 is limit ed to B cells and follicular dendritic cells (FDCs), one of these cell type s is likely to be involved, One of the suggested modes of action of IgE/CD2 3 is to increase the ability of B cells to present Ag to T cells, as demons trated to take place in vitro. Another possibility is that FDCs capture the IgE/Ag complexes and present these directly to B cells. The purpose of the present study was to determine whether CD23(+) B cells or FDCs are respons ible for the IgE/CD23-mediated enhancement of specific Ab responses in vivo . We show that the enhancement is completely restored in irradiated CD23-de ficient mice reconstituted with CD23(+) spleen or bone marrow cells. In the se mice, the B cells are CD23(+) and the FDCs are presumably CD23(-) becaus e the FDCs are radiation resistant and are reported not to be replaced by d onor cells after this type of cell transfer. In contrast, enhancement was n ot restored in irradiated wild-type mice reconstituted with CD23(-) cells. These results indicate that CD23(+) B cells, and not FDCs, are the cells th at capture IgE/Ag complexes and induce enhancement of Ab responses in vivo.