@article{oai:u-ryukyu.repo.nii.ac.jp:02016208,
 author = {花城, 和彦 and 渡慶次, 賀博 and 島田, 誠二 and 砂川, 昌範 and 中村, 真理子 and 小杉, 忠誠 and Hanashiro, Kazuhiko and Tokeshi, Yoshihiro and Shimada, Seiji and Sunagawa, Masanori and Nakamura, Mariko and Kosugi, Tadayoshi},
 issue = {3},
 journal = {琉球医学会誌 = Ryukyu Medical Journal},
 note = {The type-I allergy is mediated by the interaction between IgE and its high affinity receptor (Fc$ \varepsilon $RI) followed by cross-linking with specific allergen. The binding site for the IgE was identified on the Fc$ \varepsilon $RI $ \alpha $ subunit, and the soluble $ \alpha $ subunit of Fc$ \varepsilon $RI was effective in controlling the lgE-mediated inflammation. Recent studies using IgE knock out mice revealed that IgG could also induce anaphylaxis. However, in the Fc$ \varepsilon $RI $ \alpha $ subunit knock out mice, IgE and IgG could not induce anaphylaxis. These results demonstrated that Fc$ \varepsilon $RI expression is essential for the development of the IgE-mediated inflammation. Further investigation on the interaction between IgE and Fc$ \varepsilon $Rl $ \alpha $ subunit on the membrane of target cells and on signal transduction in the cytoplasma and nucleus should offer novel concepts in developing strategies for the treatment of IgE-mediated inflammation., 論文},
 pages = {117--127},
 title = {[総説］I型アレルギーにおけるIgEとその受容体Fc$ \varepsilon $RIの相互反応},
 volume = {20}
}