Regulation of high-affinity IgE receptor-mediated mast cell activation by murine low-affinity IgG receptors.

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Regulation of high-affinity IgE receptor-mediated mast cell activation by murine low-affinity IgG receptors.

Allergic symptoms result from the release of granular and lipidic mediators and of cytokines by inflammatory cells. The whole process is initiated by the aggregation of mast cell and basophil high-affinity IgE receptors (Fc epsilon RI) by IgE and antigen. We report here that IgE-induced release of mediator and cytokine can be inhibited by cross-linking Fc epsilon RI to low-affinity IgG receptor...

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Role of IgE Low-Affinity Receptor (CD23) in Pathogenesis of Nasal Polyp

Background: Nasal polyps, a common clinical problem, are characterized by eosinophilic and mast cell inflammation.  The role of allergy and IgE in pathogenesis of nasal polyps is still unclear.  IgE receptors are important components of the immunological pathway in allergic and inflammatory diseases. Objective: To determine if the low affinity IgE receptor (CD23) is presented on nasal polyp tis...

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Human eosinophils and human high affinity IgE receptor transgenic mouse eosinophils express low levels of high affinity IgE receptor, but release IL-10 upon receptor activation.

FcepsilonRI expressed by human eosinophils is involved in IgE-mediated cytotoxicity reactions toward the parasite Schistosoma mansoni in vitro. However, because receptor expression is low on these cells, its functional role is still controversial. In this study, we have measured surface and intracellular expression of FcepsilonRI by blood eosinophils from hypereosinophilic patients and normal d...

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Rictor negatively regulates high-affinity receptors for IgE-induced mast cell degranulation.

Rictor is a regulatory component of the mammalian target of rapamycin (mTOR) complex 2 (mTORC2). We have previously demonstrated that rictor expression is substantially downregulated in terminally differentiated mast cells as compared with their immature or transformed counterparts. However, it is not known whether rictor and mTORC2 regulate mast cell activation. In this article, we show that m...

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ژورنال

عنوان ژورنال: Journal of Clinical Investigation

سال: 1995

ISSN: 0021-9738

DOI: 10.1172/jci117701