Enhancement of IgE-mediated histamine release from human basophils by viruses: role of interferon

How interferon enhances histamine release is not clear. It is known that in preparations of human leukocytes, histamine is present only in basophils. These basophils have specific receptors for IgE and such receptors are not present on other leukocytes (19, 27) . The release of histamine is triggered by the bridging of two IgE molecules on the basophil surface (28) . The reaction can be initiated by either ragweed antigen E or anti-IgE and the two mechanisms appear identical (29) . The release of histamine from the cell is a secretory process and does not result in cell death. This secretory process is modulated by the level of intracellular cyclic AMP, and agents such as isoproterenol, prostaglandin E, cholera toxin, or theophylline, which raise intracellular levels of cyclic AMP, will inhibit the release of histamine. Agents which either decrease cyclic AMP levels (e.g., imidazole, a-adrenergic compounds, PGF~), or increase cyclic GMP levels (e.g., exogenous cyclic GMP, carbamylcholine) have been reported to enhance histamine release from lung mast cells (30, 31) , but thus far not from peripheral basophils (32) . Microtubules and microfilaments also play a role in this secretory process; colchicine, which inhibits microtubular aggregation, inhibits the release reaction. Heavy water, which in many systems promotes microtubular aggregation, enhances histamine release and also reverses the action of colchicine (33, 34) . Cytochalasin B, an agent known to disrupt microfilaments, also will enhance the IgE-mediated histamine release reaction (34) (35) (36) . Whether or not interferon enhances histamine release by altering cyclic nucleotide levels, promoting microtubule aggregation, disrupting microfilaments, or some other mechanism remains to be determined.