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pubmed:abstractText |
SFA and EFA are derived from distinct mouse T cell hybridomas secreting one or the other (but not both) factor, and although both are capable of inhibiting FcR epsilon expression by unfractionated spleen cells induced by monomeric IgE, neither was inhibitory for EIRT-induced FcR epsilon expression by T cells in the same cell population. This suggests that the final target cell for the inhibitory effects of SFA and EFA is the FcR epsilon+ B lymphocyte. T cells are required for both SFA- and EFA-mediated FcR epsilon inhibition, and more precisely, as shown in this study, SFA stimulates Lyt-1+ cells in the presence or absence of IgE to produce a suppressive effector molecule (SEM), and EFA together with IgE stimulates Lyt-2+ cells to produce an enhancing effector molecule (EEM), both of which can directly inhibit FcR epsilon expression by B cells. SFA and SEM can inhibit both IgE- and EIRB-induced FcR epsilon expression by B cells, indicating that SFA may act by blocking the EIRB-mediated expansion of the FcR epsilon+ B cell population. EFA and EEM, in contrast, can inhibit IgE-induced but not EIRB-induced FcR epsilon expression, indicating that EFA may act at some point before the release of EIR, perhaps involving those FcR epsilon+ B cells that respond to IgE and produce EIRB. Finally, although neither SFA and EFA display IgE binding properties, both SEM and EEM, in contrast, are IgE binding factors (IgE-BF) and may be homologous to the suppressive IgE binding factor and potentiating IgE binding factor described by other investigators. The possible interrelationships between these various cells and factors are discussed.
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