INHIBITION OF IGE AND COMPOUND 48-80-INDUCED HISTAMINE-RELEASE BY LECTINS

  • 1 January 1975
    • journal article
    • research article
    • Vol. 29  (2) , 371-386
Abstract
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. Histamine release in an Ig[immunoglobulin]E-mediated and a compound 48/80[p-methoxy-phenethyl methylamine formaldehyde product]-mediated reaction was inhibited in cells which were pretreated with these lectins. With concanavalin A and the R. communis lectin both effects were prevented by the addition of the appropriate monosaccharides to the incubations. 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, specifically inhibited histamine release which was caused by the lectin from R. communis without affecting the inhibition of IgE-mediated histamine release. 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 direct histamine release. Furthermore, the nominally galactose-specific lectins from Sophora japonica and Ulex europaeus 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, D-galactose, .alpha.-linked, intrachain D-glucose (or mannose) and N-acetylglucosamine residues but probably not N-acetyl-galactosamine, 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.