It was recently demonstrated that FDCs, which are crucial for the maintenance of GCs and FO architecture, express type I IFN through a TLR-7 pathway upon internalizing complement-opsonized self-immune complexes through the complement receptor CD21 in the 564Igi RNP-specific lupus mouse model; this pathway is important for spontaneous GC formation and production of isotype-switched autoantibodies (210). The gene discussed is TLR7; the disease is systemic lupus erythematosus.