Mechanisms of reaginic hypersensitivity and immunotherapy

Abstract

Reaginic antibodies in hay fever patients belong to IgE. The immunoglobulin sensitizes basophilic granulocytes and mast cells from homologous species and mediates the release of chemical mediators which cause allergic symptoms. The sensitization is due to the binding of IgE to receptors on the target cells through the Fc portion of the molecules. High affinity of the molecules for the receptor is responsible for the biologic activity of IgE antibodies and for the persistence of sensitization with the antibodies. The initial step of the reaginic hypersensitivity reactions is bridging of cell-bound IgE antibody molecules by a multivalent antigen. Since IgE is firmly bound with receptors, cross-linkage of IgE molecules will cause a disturbance of membrane structure and/or interaction between receptor molecules at the cell membrane, which will activate membrane-associated enzymes. It appears that the activation of sequences of enzymes will lead to the release of chemical mediators from the cells. In view of the role of IgE antibodies in allergic diseases such as hay fever, attempts were made to depress the IgE antibody response to allergen. A experimental model in the mouse indicated that the generation of antigen-specific suppressor T cells is involved in the depression of IgE antibody formation by immunotherapy.