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 Th cell-induced CD23 expression defines a distinct subset of human B cells, allospecific Th cells 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 Th cells. 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 Th cells. We utilized the CD23 induction assay to investigate a potential synergistic effect in B cell activation mediated by Th cell 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 Th cell 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 Th cell proliferation is a property of the low density B cell population. These results suggest that the antigen-specific interaction between Th cells and resting B cells may serve to activate the B cell in preference to the T cell. © 1989.
Jover, J. A., Chartash, E. K., Kushner, B., Friedman, S. M., & Crow, M. K. (1989). T helper cell-induced CD23 (BLAST-2) expression: An activation marker for the high density fraction of human B cells. Clinical Immunology and Immunopathology, 53(1), 99–112. https://doi.org/10.1016/0090-1229(89)90105-0