T helper cell-induced CD23 (BLAST-2) expression: An activation marker for the high density fraction of human B cells

  • Jover J
  • Chartash E
  • Kushner B
 et al. 
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We previously reported that the coculture of cloned, allospecific human T helper (Th) cells with allogeneic B cells bearing the relevant major histocompatibility complex class II antigen induces expression of the B cell activation antigen CD23 (BLAST-2) on a fraction of the B cells. To determine if Thcell-induced CD23 expression defines a distinct subset of human B cells, allospecific Thcells were cultured with B cell fractions isolated on discontinuous Percoll gradients. Our results show that the majority of high density resting B cells, those bearing surface IgD and little of the 4F2 activation antigen, express high intensity CD23 after culture with relevant allospecific Thcells. Essentially all of the low density, presumably in vivo-activated, B cell subpopulation and a fraction of the high density B cell pool remain CD23 negative after repeated culture with relevant allospecific Thcells. We utilized the CD23 induction assay to investigate a potential synergistic effect in B cell activation mediated by Thcell signaling and antigen analog-induced cross-linking of B cell surface Ig receptors. These studies show that phorbols known to result in PKC activation, one of the biochemical consequences of sIg-mediated B cell signaling, enhance both the intensity of CD23 expression and the percentage of cells expressing CD23 after allospecific Thcell or IL-4 interaction with high density, but not low density B-cells. Finally, we show that while Th-induced B cell activation, as measured by CD23 expression, is a property of high density B cells, induction of Thcell proliferation is a property of the low density B cell population. These results suggest that the antigen-specific interaction between Thcells and resting B cells may serve to activate the B cell in preference to the T cell. © 1989.

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  • Juan A. Jover

  • Elliot K. Chartash

  • Barbara Kushner

  • Steven M. Friedman

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