BACKGROUND: Immediate hypersensitive reactions induced by buckwheat ingestion are considered to be IgE-mediated. Some subjects, however, develop no immediate adverse reactions after buckwheat ingestion despite high levels of buckwheat-specific antigens IgE. The mechanism is unknown. OBJECTIVE: To investigate the mechanisms. METHODS: RAST for buckwheat and rice and RAST inhibition between these antigens were performed using sera from 23 buckwheat-sensitive subjects and 30 buckwheat-tolerant subjects who had IgE antibodies for both buckwheat and rice. RESULTS: RAST values for buckwheat and rice were significantly correlated with each other (P < .01) in the buckwheat-tolerant group, but not in the buckwheat-sensitive group. This suggests the IgE antibodies from the subjects without any overt symptoms after buckwheat ingestion recognize the cross-reactive epitope between buckwheat and rice, whereas the IgE antibodies from those with immediate reactions to buckwheat ingestion do not. RAST inhibition assays were performed to evaluate this. RAST inhibition of heterogeneous combination of inhibitor and disc antigen such as rice and buckwheat was significantly smaller than that of homologous combination of rice and rice or buckwheat and buckwheat in the group with immediate symptoms after buckwheat ingestion. There was no significant difference in RAST inhibition between homologous and heterogeneous combinations in the group without the symptoms. CONCLUSIONS: There was cross-reactivity with IgE antibodies between buckwheat and rice and IgE antibodies from the buckwheat-tolerant subjects with high levels of IgE antibodies from the buckwheat might recognize the epitopes on buckwheat antigens which cross-react with rice antigens, whereas IgE antibodies from the buckwheat-sensitive subjects might bind to buckwheat-specific epitopes.
BACKGROUND: Immediate hypersensitive reactions induced by buckwheat ingestion are considered to be IgE-mediated. Some subjects, however, develop no immediate adverse reactions after buckwheat ingestion despite high levels of buckwheat-specific antigens IgE. The mechanism is unknown. OBJECTIVE: To investigate the mechanisms. METHODS: RAST for buckwheat and rice and RAST inhibition between these antigens were performed using sera from 23 buckwheat-sensitive subjects and 30 buckwheat-tolerant subjects who had IgE antibodies for both buckwheat and rice. RESULTS: RAST values for buckwheat and rice were significantly correlated with each other (P < .01) in the buckwheat-tolerant group, but not in the buckwheat-sensitive group. This suggests the IgE antibodies from the subjects without any overt symptoms after buckwheat ingestion recognize the cross-reactive epitope between buckwheat and rice, whereas the IgE antibodies from those with immediate reactions to buckwheat ingestion do not. RAST inhibition assays were performed to evaluate this. RAST inhibition of heterogeneous combination of inhibitor and disc antigen such as rice and buckwheat was significantly smaller than that of homologous combination of rice and rice or buckwheat and buckwheat in the group with immediate symptoms after buckwheat ingestion. There was no significant difference in RAST inhibition between homologous and heterogeneous combinations in the group without the symptoms. CONCLUSIONS: There was cross-reactivity with IgE antibodies between buckwheat and rice and IgE antibodies from the buckwheat-tolerant subjects with high levels of IgE antibodies from the buckwheat might recognize the epitopes on buckwheat antigens which cross-react with rice antigens, whereas IgE antibodies from the buckwheat-sensitive subjects might bind to buckwheat-specific epitopes.