Abstract
The pathophysiological significance of histaminergic receptors located on the membranes of immunocompetent cells is reviewed. H2-receptor agonists decrease the immunological histamine release from isolated serosal mast cells and from isolated hearts taken from actively sensitised guinea-pigs. Histamine and H2-receptor agonists inhibit the generation of superoxide anion from human neutrophils activated by FMLP and by substance P. These observations lend further support to the hypothesis of an immunodepression exerted by the activation of H2-receptors, which can be converted to immunostimulation by treatment with H2-receptor antagonists.
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