Immune response against the T-independent antigen alpha (1----3) dextran. II. Occurrence of B gamma memory cells in the course of immunization with the native polysaccharide is T cell dependent.

The immune response of BALB/c mice against the bacterial antigen dextran B1355S [alpha (1----3)dextran] (Dex), a class 2 T cell-independent antigen, is largely restricted to IgM class antibody production. However, despite the fact that Dex fails to give rise to enhanced IgG responses upon repeated immunization, the development of Dex-specific B gamma memory cells, i.e. resting B cells committed to the production of specific IgG antibodies, is observed upon immunization with Dex. These B gamma memory cells, albeit not activated to IgG production in situ, can be activated upon adoptive transfer into irradiated congenic BALB Ighb mice. This mouse strain is a nonresponder strain to Dex. The expression of adoptively transferred Dex-specific B gamma memory cells is T cell-independent as T cell depletion of spleen prior to cell transfer into BALB.Ighb recipients does not abolish the IgG response. Dex-primed athymic BALB/c nude mice, in contrast to euthymic mice, give a pronounced primary IgG response but do not develop Dex-specific B gamma memory cells. Yet, they do so when reconstituted with syngenic T cells prior to immunization. This indicates that the formation of Dex-specific B gamma memory cells requires the presence of functional T cells. The pronounced primary IgG anti-Dex response of nude mice is greatly impaired by T cell reconstitution. Thus, with regard to T cell dependence, there is an inverse relationship between the formation of B gamma memory cells and the capacity to produce IgG anti-Dex. Dex-specific B gamma memory cells from BALB/c mice are expressed in congenic BALB.Ighb recipients (nonresponder to Dex) but not when transferred into identically treated syngenic hosts. This also applies to memory cells from Dex-primed female (CBA/N X BALB/c)F1 [NBF1] or from (BALB/c X CBA/N)F1 hybrids. Dex-specific B gamma memory cells from these donors are demonstrable upon adoptive transfer into BALB.Ighb mice, but they are not expressed when transferred into syngenic recipients, including male NBF1 hybrids. NBF1 males, albeit possessing the VH-Dex+ allele, do not mount humoral responses to Dex, a deficiency which is ascribed to an X chromosome-linked B cell defect. The apparent absence of Dex-specific antibodies in NBF1 males provides an opportunity to examine whether B gamma memory cell expression is inhibited in syngenic recipients by anti-Dex or autologous anti-idiotype antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)