Demonstration of Antigen on the Surface of Sensitized Rat Mast Cells

Abstract

IT is generally accepted that passive cutaneous anaphylaxis (PCA) is due to an interaction of antigen with antibody “fixed” to tissues or cells, followed by the release of pharmacologically active substances, particularly histamine¹. Recent experiments have shown, however, that two different pathogenetic mechanisms may be operating in PCA in both rats² and guinea-pigs³, depending on the type of antibody used for sensitization. In the rat, PCA induced by rabbit hyperimmune antibody cannot be suppressed by antihistamine, which has suggested that PCA and the Arthus reaction “may be linked by a common aetiological factor” (ref. 4). This “factor” may be related to alterations produced by polymorphonuclear leucocytes, because this type of PCA can be suppressed by rendering rats neutropenic². In PCA of normal rats, polymorphonuclear leucocytes phagocytose antigen-antibody complexes, become degranulated and presumably release their lysosomal contents, just as they do in vitro⁵. On the other hand, the PCA reaction in the rat induced by “mast cell sensitizing” or “anaphylactic” antibody can bo inhibited by a combination of antihistamine and antiserotonin (BOL-148) (ref. 6), and this has led to the suggestion that “anaphylactic” antibody is fixed on the surface of mast cells and that when it interacts with antigen the mast cell is disrupted and the pharmacologically active amines released. Against this hypothesis has been opposed, on the basis of studies with red cells as antigen, the suggestion that the interaction of antigen and antibody occurs on the inner aspect of endothelial cells^7,8. Because red cells would not readily pass across the endothelial barrier, it was argued that the combination of antigen and antibody occurs within the lumen of the vessel. We have carried out an electron microscope investigation of PCA in an attempt to resolve some of these controversies.