The systemic immune response of joining-chain (J-chain)-deficient mice (J(-/-) mice) on a C57BL/6 background against the hapten 4-hydroxy-3-nitrophenyl (NP) was analysed. While primary IgG responses to the hapten were similar to those observed in WT control animals, secondary immune responses were compromised both at the level of serum IgG and the number of responding B cells. The repertoire switch from lambda to kappa in secondary immune responses was diminished in J(-/-) mice. The number of somatic mutations introduced in the V(H) 186.2 gene during the primary immune response was reduced, while the frequency of affinity-increasing mutations in position 33 was similar. By adoptive transfer experiments it could be shown that the compromised secondary immune response was transferred with T cells from J(-/-) mice. Thus, J-chain-deficient mice have a selective defect in T helper cell function during B cell immune responses, resulting in a deficiency in the formation of B cell memory.