• 1 January 1977
    • journal article
    • research article
    • Vol. 33  (1) , 31-40
Abstract
Adult thymectomized, repopulated mice were chronically depleted of circulating C3 [complement component 3] by treatment with cobra venom factor after primary immunization with dinitrophenylated [keyhole limpet] hemocyanin (DNP-KLH). This treatment totally abrogated the development of B[bone marrow derived]-cell memory in such mice, as assayed by a co-operative lymphocyte transfer. The failure of memory development appeared to involve impaired precursor proliferation following priming. The localization of DNP-KLH in splenic lymphoid follicles was antibody- and C3-dependent; thymus-deprived mice made sufficient antibody to DNP-KLH to effect follicular localization of the antigen. These and earlier observations suggest that the development of B-memory cells involves the formation of antigen-antibody-C3 complexes on dendritic cells in lymphoid follicles. C3 may stabilize the antigen bridge between dendritic cells and virgin precursors. C3 depletion had little effect on the functional expression of primed B cells, thus suggesting that only the early stages of B-cell triggering are C3 dependent.