Lymphocytes bearing Fc receptors for IgE. VII. Possible participation of phospholipase A2 in the glycosylation of IgE-binding factors.

Abstract

Previous experiments have shown that IgE induced an increase in the proportion of FcϵR(+) cells and formation of IgE-binding factors in both normal and Con A-activated cell cultures. The IgE-binding factors formed by 1 jug/ml Con A-activated cells failed to bind to Con A-Sepharose and selectively suppressed the IgE response. The present experiment shows that both melittin, an activator of phospholipase A2, and monoclonal antibody against a phospholipase A2 inhibitory protein enhanced the IgE-induced increase in FcϵR(+) cells and changed the nature of IgE-binding factors formed. Thus, IgE-binding factors formed by the Con A-activated cells in the presence of either melittin or the monoclonal antibody selectively enhanced the IgE response, and had affinity for Con A. The same agents were used to modulate the formation of IgE-binding factors by lymphocytes from CFA-treated rats, which spontaneously released IgE-suppressive factors. These lymphocytes released IgE-potentiating factors upon incubation with either melittin or the monoclonal antibody. The results indicate that activation of phospholipaseA2 enhanced the glycosylation of IgE-binding factors, and that glycosylation is essential for the ability of the factors to potentiate the IgE response. Lysophosphatidyl choline and its analogues also induced the conversion of IgE-suppressive factors to IgE-potentiating factors. These results suggest that the formation of lysolecithin by activation of phospholipase A2 induced enhancement of glycosylation of IgE-binding factors. DNA synthesis of T cells is required neither for the formation of IgE-binding factors nor for switching from the formation of IgE-suppressive factor to IgE-potentiating factor. The results suggest strongly that the same cells have capacities to form both types of IgE-binding factors and that the biologic activity of IgE-binding factors formed by the activated T cells is decided during the process of glycosylation of the same precursor molecules.