To investigate the role of helminth-induced IgE in the worm-atopy relationship, the levels of IgE directed against helminthic antigens (Ascaris, Echinococcus, and Schistosoma)and total IgE were determined by radioimmunoassay in the sera of 106 atopic subjects, using extrinsic allergen-specific IgE. Ten patients were found to have detectable levels of helminth-specific IgE antibodies. The total IgE levels in these patients were approximately five-fold greater than those in patients with no detectable helminth-specific IgE. The differences were highly significant (P <0.005). The results indicate that atopy could develop in individuals with parasite-specific IgE antibodies and that helminthic antigens strongly potentiate IgE-secreting plasma cells. Atopic diseases and helminthic infections are associated with a similar IgE immune response, namely, an increased serum level of polyclonal (total) IgE antibodies. [1][2][3][4][5][6][7][8][9][10][11][12][13][14] This association has led to conflicting hypotheses. Many reports have suggested that IgE production induced by parasitic infection protects against atopic reactions by saturating the Fc receptor for IgE on mast cells with nonspecific (irrelevant) IgE antibodies. [15][16][17] It has been shown that most of the increased total IgE content in helminth-infected individuals is nonspecific, whereas only a small portion of the induced IgE is specific to the helminthic antigens. 4,5,12,18 The binding of the allergens to the V region of immunoglobulins and the cross-linking of IgE molecules cause degranulation of mast cells, with ultimate release of histamine and other vasoactiveamines. Helminth-induced nonspecific IgE for which no antigen is available competes with allergen-specific IgE for Fc receptor sites on mast cells, thus interfering with the binding of IgE to extrinsic allergens. 15,17,20,21 This process inhibits subsequent development of allergic reactions. Other reports have suggested that parasite-induced IgE does not protect against allergic reaction because of the high turnover of IgE on mast cells, and that helminth-induced nonspecific IgE is too small to block all Fc receptor sites on mast cells. [22][23][24][25][26][27] This article assesses the prevalence of helminth-specific IgE among atopic subjects with nonhel-minthic allergen-specific IgE. In addition, serum levels of polyclonal (total) IgE were determined in atopic subjects with and without helminth-specific IgE.