B cell-intrinsic type I interferon signaling contributes to defective antibody responses to a model antigen during persistent LCMV infection.

During persistent LCMV infection, Laulhé et al. reveal that B cell-intrinsic type I interferon (IFN-I) signaling drives defective affinity maturation. Although IFN-I acts directly within B cells, its absence alone fails to restore normal humoral responses, indicating that additional extrinsic mechanisms cooperate to sustain dysfunction.