Mechanisms of reaginic hypersensitivity: a review

Gamma E antibodies represent the major part of human reaginic antibodies. The antibodies sensitize human and monkey skin, human leucocytes and primate lung tissues. The allergen‐γE antibody reaction mediates the release of histamine from human leucocytes and both histamine and SRS‐A from monkey lung tissues. The immunoglobulin is formed in lymphoid tissues especially those In respiratory and gastrointestinal tracts. Turnover rate of this protein in the blood is only 2–3 days, suggesting that human reaginic antibodies are being formed continuously in atopic patients. However, γE injected into normal skin sites is retained for a long time. The half‐time of loss of the immunoglobulin was 9–14 days in human skin and 8–10 days in monkey skin. Evidence has accumulated that IgE combines with target cells through the Fc portion of the molecules. The Fc fragments block passive sensitization of human skin with reaginic antibodies and passively sensitize human leucocytes and monkey lung tissue for reversed type reactions. Target cells in human leucocytes were identified as basophil leucocytes. The immunoglobulin binds with tissue mast cells upon passive sensitization. The initial step in reaginic hypersensitivity seems to be the bridging of cell‐bound IgE with allergen. It appears that the interaction between the IgE molecules or consequent structural changes in the Fc portion of the molecules may induce enzymatic sequences leading to the release of histamine and SRS‐A. The enzyme activated by the allergen‐γE antibody reaction is not the complement system. The biochemical pathways subsequent to the γE‐γE interaction and prior to the release of chemical mediators are unknown. However, evidence has accumulated that the β adrenergic system or the intracellular accumulation of cyclic‐AMP regulate the biochemical pathways.