Allogeneic carrier-specific enhancement of hapten-specific secondary B-cell responses.

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Abstract
The capacity of carrier-specific T [thymus-derived] cells to enhance the immune response of hapten-specific secondary B [bone marrow-derived] cells which do not share genes in the H-2 complex with the T cells was analyzed. The in vitro splenic focus technique was used. This technique allows assessment of monoclonal responses of B cells isolated in splenic fragment cultures of irradiated reconstituted carrier-primed mice. A previous report demonstrated that syngeny in the I region of the H-2 complex was necessary between the collaborating hapten-specific primary (nonimmune) B cells and carrier-specific T cells for responses yielding IgG1 [immunoglobulin G1] but not IgM antibody. The expression of I-region gene products on the surface of primary B cells and I-region syngeny with collaborating carrier-specific T cells were apparently essential elements in the triggering events leading to IgG1 synthesis by primary B cells. The results indicate that, unlike primary B cells, the majority of secondary B cells can be stimulated to produce IgG1 antibody in carrier-primed allogeneic recipients. Although the enhancement of secondary IgG1 responses is slightly greater with syngeneic T cells, the allogeneic collaborative interaction requires carrier priming of recipient mice and stimulation with the homologous hapten-carrier complex, and thus appears to be specific. These findings discriminate secondary from primary B cells, and indicate that the mechanism of stimulation of secondary B cells to yield IgG1-producing clones differs fundamentally from the stimulation of primary B cells in that the requisite for I-region syngeny is obivated.