Follicular dendritic cells (FDCs), as accessory cells to B cells, promote germinal center (GC) development. Age-related defects in the role of FDCs are well documented in vivo. In old mice, FDCs bind fewer immune complexes (ICs) and produce few iccosomes for endocytosis by B cells, antigen processing, and presentation to T cells. We recently studied whether these defects are due to changes in the FDC microenvironment or to changes in FDCs and their surface molecules. In vitro evidence suggests that age-related defects in both B cell stimulation via the BCR and co-stimulation via CD21/CD21L are related to IC-trapping by FDCs in vivo-a defect which is repairable, at least, in vitro.