Discordance between IgA B cell precursors and the secretion of IgA antibody to bacterial polysaccharides.

Abstract

B cell precursors of IgA antibody forms cells (AFC) with specificity for antigenic determinants common in the mouse environment originate in Peyer’s patches (PP) and migrate, via lymphatic ducts of the gut-associated lymphoid tissue (GALT) to mesenteric lymph nodes (MLN), and via the systemic circulation to distal mucosal secretory sites, to differentiate to IgA producing cells. It is thought that the commitment of B cell precursors to IgA production may be due to the effect of the PP microenvironment on the B cells (1,2), and the frequency of distribution of these precursors of IgA AFC show a relationship to the lymphoid tissue site in which the B cells differentiate (2–4). The mechanisms involved in the IgA cell cycle in the distal tissues and the signals triggering the differentiation of precursor B cells into IgA AFC remains less than clear. The regulation of IgA production by GALT T cells is well documented (2,5,6), and generation of IgA plaque-forming cells (PFC) to bacterial polysaccharides (Ps) is clearly T cell-dependent (TD) (2). However, the role of T cells in the IgA precursor cycle and the T cell contribution to IgA systemic antibody (Ab) to bacterial Ps have only been partly clarified (2,3,7,8).