TY - JOUR
T1 - Failure of the putative ige pentapeptide to compete with ige for receptors on basophils and mast cells'
AU - Bennich, Harts
AU - Ragnarsson, Ulf
AU - Johansson, S.
AU - Ishizaka, Kimishige
AU - Shizaka, Teruko
AU - Levy, David A.
AU - Lichtenstein, Lawrence M.
PY - 1977
Y1 - 1977
N2 - We have examined the claim that a pentapeptide resembling a portion of r-chain of IgE can inhibit allergic reactions by competing with IgE for basophil-mast cell IgE receptors. Four laboratories with expertise in different areas collaborated. The following was found. (1) There was no evidence, by autoradiography, that the pentapeptide could block IgE fixation to basophils or displace IgE from these cells. (2) There was no evidence, by histamine release studies that the pentapeptide could block basophil sensitization or remove IgE from actively sensitized cells. The pentapeptide, also, did not impair antigen-induced histamine release. (3) There was no evidence that the pentapeptide could block the skin test response in Prausnitz-Kustner testing with the antigen injected intradermally or orally administered. Neither the correct pentapeptide sequence from the f-chain nor the Fc" fragment of IgE impaired the P-K test. In each series of experiments, IgE myeloma protein, as a positive control, blocked the allergic response. The failure of the pentapeptide to block these reactions was observed at molar ratios of pentapeptide/lgE of 10 to 10. Our results, therefore, provide no evidence for competition between the pentapeptide and IgE. Even if there should be some weak affinity between the pentapeptide and IgE receptors on basophils or mast cells this would, by virtue of quantitative considerations, be of no clinical relevance.
AB - We have examined the claim that a pentapeptide resembling a portion of r-chain of IgE can inhibit allergic reactions by competing with IgE for basophil-mast cell IgE receptors. Four laboratories with expertise in different areas collaborated. The following was found. (1) There was no evidence, by autoradiography, that the pentapeptide could block IgE fixation to basophils or displace IgE from these cells. (2) There was no evidence, by histamine release studies that the pentapeptide could block basophil sensitization or remove IgE from actively sensitized cells. The pentapeptide, also, did not impair antigen-induced histamine release. (3) There was no evidence that the pentapeptide could block the skin test response in Prausnitz-Kustner testing with the antigen injected intradermally or orally administered. Neither the correct pentapeptide sequence from the f-chain nor the Fc" fragment of IgE impaired the P-K test. In each series of experiments, IgE myeloma protein, as a positive control, blocked the allergic response. The failure of the pentapeptide to block these reactions was observed at molar ratios of pentapeptide/lgE of 10 to 10. Our results, therefore, provide no evidence for competition between the pentapeptide and IgE. Even if there should be some weak affinity between the pentapeptide and IgE receptors on basophils or mast cells this would, by virtue of quantitative considerations, be of no clinical relevance.
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U2 - 10.1159/000231784
DO - 10.1159/000231784
M3 - Article
C2 - 67091
AN - SCOPUS:0017348317
SN - 1018-2438
VL - 53
SP - 459
EP - 468
JO - International archives of allergy and immunology
JF - International archives of allergy and immunology
IS - 5
ER -