Interrelationship of primed B cells with the potential for IgE and/or IgA expression

The relationship between the pathways of B cell differentiation leading to IgE or IgA expression was analyzed by assessing the isotype potential of primed B cells as revealed over many generations of clonal outgrowth in splenic fragment cultures. Cells from (CBA/N X BALB/C) F1 male and female mice primed with phosphocholine (PC)-hemocyanin (Hy) and given a secondary stimulus with PC-Hy or PC-determinants via an Ascaris infection gave rise to a large proportion (25-48%) of clones which expressed anti-PC IgE along with any one or mixture of other isotypes, especially IgG and/or IgA. Accompanying the appearance of these cells in the Peyer's patches following Ascaris infection was the steady rise in IgA committed cells over a 12 week period. The potential to express IgE seems to be a normal feature of the development of secondary or memory cells. The coexpression of IgE randomly with all other isotypes supports a linear rather than a branched pathway of B cell differentiation. Ascaris or PC-determinants given to F1 mice were not unique in their ability to prime cells with the potential for IgE expression. Stimulation of BALB/c mice with two low doses of N-acetyl-glucosamine-conjugated hemocyanin (GlcNAc-Hy) primed cells in vivo generated a high proportion (63%) of clones in vitro that expressed IgE and most of these exclusively coexpressed IgA (16/26) suggesting a progressive restriction in isotype potential. Cells which gave rise to IgE producing clones specific for the priming hapten did not support the expression of IgE by clones of other specificities costimulated in vitro (anti-inulin, anti-beta-galactosyl). Thus the potential to express IgE seems to be both an inherent property of the B cells and under hapten-specific or hapten-linked regulation.