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| Research article summary (published 30 Jul 1992): |
[IgE-mediated allergy and Fc epsilon receptor II]
Full Abstract
Two types of IgE receptors, Fc epsilon receptor I (Fc epsilon RI) and Fc epsilon receptor II (Fc epsilon RII), are known to be involved in IgE-mediated allergy. Fc epsilon RI is expressed on mast cells and basophils, and cross-linkage of Fc epsilon RI leads to the release of chemical mediators from these cells. Fc epsilon RI consists of alpha, beta and gamma chains, and cDNAs encoding these chains were recently cloned. Fc epsilon RII is expressed on various cells such as mature mu+delta+ B cells and activated monocytes and eosinophils. The cDNA encoding B cell Fc epsilon RII was cloned by several groups including ours, and Fc epsilon RII was found to be a single chain receptor expressed with its N-terminal inside the cells, homologous to C-type animal lectins. Subsequently, we identified two species of Fc epsilon RII, Fc epsilon RIIb, whose structures differ only at the N-terminal cytoplasmic region but share the same C-terminal extracellular region. These two receptors are generated utilizing different transcriptional initiation sites and 5' exons. Fc epsilon RIIa is constitutively expressed only on B cells. While Fc epsilon RIIb is inducible by IL-4 on B cells, monocytes and eosinophils. By employing transformants expressing Fc epsilon RIIa or Fc epsilon RIIb, it was demonstrated that Fc epsilon RIIa is involved in IgE-mediated endocytosis, whereas Fc epsilon RIIb functions in IgE-dependent phagocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Author information
Author/s: Suemura, M (M);
Affiliation: Department of Medicine III, Osaka University Medical School.
Journal and publication information
Publication Type: English Abstract; Journal Article
Journal: Nihon Kyobu Shikkan Gakkai zasshi (Nihon Kyobu Shikkan Gakkai Zasshi), published in JAPAN. (Language: jpn)
Reference: 1992-Aug; vol 30 (issue 8) : pp 1427-33
Dates: Created 1992/12/21; Completed 1992/12/21; Revised 2006/11/15;
PMID: 1434215, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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