Changes in specific B cells and the dissemination of the primed state in vivo following antigenic stimulation by different mucosal routes.

Immunologic dogma holds that the adaptive and long-term potential of the antibody response is fashioned by antigen-dependent, selective clonal proliferation of specific B cells and the retention of some which may undergo a second round of antigen-stimulated clonal expansion with antibody production. Apparently, the short-term, immediate consequences of an antibody response depend on the mix of isotypes displayed in vivo upon exposure to antigen. This latter seems to be clearly regulated by T cells, but it is also likely that the isotype potential of a B cell population and its future possible display of isotypes is linked to the initial, antigen-dependent proliferative phase in the development of an antibody response. In vitro analysis at limiting dilutions of specific B cells primed in vivo has led to the operational definition of IgA-committed cells. These B cells increase in frequency following chronic or acute antigenic stimulation of gut mucosa and have the potential to proliferate again in the presence of antigen and TH(Ag) cells to produce exclusively IgA. A general relationship exists between mucosal or parenteral priming of B cells and their potentials to express IgA and/or IgE--both isotypes appear to be likely products of secondary B cells and frequently both can be expressed by the same clone activated by a second-round of T-dependent antigenic stimulation. Cross priming--exposure of GALT or BALT leading to secondary B cells in the opposite mucosal lymphoid tissue--suggests an inherent antagonism between development of allergic (IgE) and putative allergy blocking (IgA) potentials.(ABSTRACT TRUNCATED AT 250 WORDS)