Murine B-cell stimulatory factor 1 (interleukin 4) increases expression of the Fc receptor for IgE on mouse B cells.

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Abstract
We have studied the activity of mouse B-cell stimulatory factor 1 (interleukin 4, IL-4) on resting splenic B cells and on a B-cell hybridoma. Purified T-cell-derived as well as recombinant IL-4 was shown to increase the expression of the low-affinity Fc receptor for IgE (Fc.epsilon.R) on a majority of B lymphocytes in a 24-hr culture period. Levels of Fc .epsilon. R expression increased 2- to 3-fold on splenic B cells and up to 6-fold on a B-cell hybridoma. The effect was inhibited by an anti-IL-4 monoclonal antibody and by mouse .gamma.-interferon. Other recombinant lymphokines exhibited no effect on either Fc.epsilon.R expression or the induction by IL-4. The presence of IgE during the stimulation with IL-4 resulted in an additional increase in Fc.LAMBDA.eR expression. These data and results showing that IgE prevents Fc.epsilon.R turnover while IL-4 increases the rate of Fc.epsilon.R synthesis suggest that the mechanisms by which IgE and IL-4 increase Fc.epsilon.R expression are likely to be different. The starting population of splenic B cells expressed low levels of Fc.epsilon.R and was relatively uniform in size (small). After > 48 hr of culture with IL-4, viable b cells had not undergone DNA synthesis and consisted mainly of larger highly Fc.epsilon.R-positive cells (23%) and medium-sized Fc.epsilon.R-positive cells (60%). A possible role for Fc.epsilon.R in certain B-cell maturation pathways is discussed.