Immediate immunoglobulin E (IgE)-mediated or type I (Coombs and Gell, 1975) hypersensitivity, sometimes referred to simply as “allergy,” is an extra ordinarily widespread disease, said to affect approximalely 10% of Caucasian populations al any one time. The form of immediate hypersensitivity most com-monly encountered is allergic rhinitis, although more severe hypersensitivity reactiuns are seen, for example, in allergic asthma and systemic anaphylaxis. The clinical signs of type I allergic reactions seen in man and other animals, namely, local inflammation and swelling, mucous production, airways obstruc-tion, and shock are produced by release of granule-associated vasoactive media-tors such as histamine, slow-reacting substance of anaphylaxis, and other active components (Austen et al., 1975; Goetz] and Austcn, 1977). These substances, at least some of which have pronounced effects on smooth muscle, secretions, vascular permeability, and Chemotaxis of eosinophils, are released from basophils and mast cclls following interaction of antigcn with complementary IgE antibodies fixed to the cell surfaccs (Ishizaka et al., 1970a). The IgE molecules (Ishizaka et al., 1966; Bennich and Johansson, 1967; Ishizaka 1975) function in this process by their capacity to bind both to the mast cell or basophil surface via the Fe piece of the antibodies (Stanworth et al., 1968; Ishizaka et al., 1970b) and to the complementary antigen via the antibody-combining Sites. Multivalent but not Univalent antigens initiate mediator release demonstrating that cross-linking of the cell-bound IgE is necessary to trigger the cells (Mossmann et at., 1974; Siraganian et al., 1975).