Induction of the high-affinity IgE receptor (FcɛRI) on human mast cells by IL-4
The high-affinity IgE receptor (FceRI) is necessary for the induction of IgE-mediated allergic reactions. Cross-linking of FcɛRI expressed on mast cells causes the release of various inflammatory mediators, which trigger allergic reactions. Recently, mast cells lacking FcɛRI have been observed in vi...
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Published in | International immunology Vol. 8; no. 9; pp. 1367 - 1373 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Oxford University Press
01.09.1996
Oxford Publishing Limited (England) |
Subjects | |
Online Access | Get full text |
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Summary: | The high-affinity IgE receptor (FceRI) is necessary for the induction of IgE-mediated allergic reactions. Cross-linking of FcɛRI expressed on mast cells causes the release of various inflammatory mediators, which trigger allergic reactions. Recently, mast cells lacking FcɛRI have been observed in vivo and in vitro, suggesting the presence of regulational mechanisms in the induction of FcɛRI. In this report, we demonstrate that IL-4 up-regulates FcɛRI in cultured human mast cells, which are grown from cord blood mononuclear cells in the presence of steam cell factor and IL-6, and usually lack FcɛRI expression. At the protein level, the induction of FcɛRI was observed by flow cytometric analysis and the induced FcɛRI expression was stable for at least 23 days in the presence of IL-4. Consistently, Northern blot analysis demonstrated the increase of α chain mRNA of FcɛRI and revealed that the up-regulation of FcɛRI occurred at the transcriptional level. FcɛRI induced by IL-4 was functional and caused histamine and β-hexosaminidase release from mast cells upon cross-linking. Taken together, these results indicate a new role of IL-4 in allergic reactions, besides the stimulation of IgE production. |
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Bibliography: | ArticleID:8.9.1367 Correspondence to H. Toru ark:/67375/HXZ-6BWH7RF2-C istex:C14F6EF46056660C3BA2CF11440BE6D523404034 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0953-8178 1460-2377 |
DOI: | 10.1093/intimm/8.9.1367 |