Inhibition of IgE and compound 48/80-induced histamine release by lectins.

Lectins from Ricinus communis and Glycine max, as well as wheat germ agglutinin and concanavalin A, caused a dose-dependent release of histamine from mast cells present in the mixed peritoneal cells from the rat. In addition, histamine release in an IgE-mediated and a compound 48/80-mediated reaction was inhibited in cells which had been pretreated with these lectins. With concanavalin A and the R. communis lectin both effect were prevented by the addition of the appropriate monosaccharides to the incubations. However, the lectin-induced histamine release and the lectin-induced inhibition of subsequent IgE-mediated histamine release could be dissociated: thus L-rhamnose, a hexose not ordinarily found on mammalian cell membranes, a specifically inhibited histamine release which was caused by the lectin from R. communis without affecting the inhibition of IgE-mediated histamine release. Conversely, D-fucose, which also is not a constituent of cell membrane glycolipids or glycoproteins prevented the inhibition of IgE-mediated histamine release by this lectin without affecting the lectin-induced histamine release. Furthermore, the nominally galactose-specific lectins from Sophora japonica and Ulex europeus inhibited IgE-mediated histamine release while causing little if any histamine release themselves. High concentrations of the lectin from Lotus tetragonolobus failed to cause histamine release or to affect the IgE-mediated histamine release reaction. Based on the known structural specificity of these lectins and the amounts of the lectins which were required to demonstrate an effect, it was concluded that D-galactose, alpha-linked, intrachain D-glucose (or mannose), and N-acetylglucosamine residues but probably not N-acetyl-galactosamine or L-fucose residues in the glycolipids or glycoproteins of the mast cell membrane can play a role in the initiation of histamine release and in the desensitization of the cells to subsequent histamine release-inducing stimuli.