Abstract
THE mechanism of cell destruction in allergic inflammation is not well understood. Two explanations for production of cell damage have, however, been proposed: (a) that the antigen-antibody reaction causes, in some non-specific manner, permeability changes in cells which result in the release of active mediators of inflammation (histamine, etc.) and that the latter are directly involved in the allergic process1; (b) that the antigen-antibody reaction activates proteolytic enzymes (plasmin, proteases) that injure the cells2–4.
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