Abstract |
Mast cells and basophils, which are activated by immunoglobulin E ( IgE) and allergen, play a prominent role in anaphylaxis. However, they express at least three types of IgE receptor, including the high affinity IgE receptor ( Fc epsilon RI). The relative contribution of these IgE receptors, and possibly other receptors such as Fc epsilon RII/CD23 and Mac-2, to the genesis of in vivo anaphylaxis is still unclear. To address this question, we have generated Fc epsilon RI-deficient mice. These mice appear normal and express a normal number of mast cells, but they are resistant to cutaneous and systemic anaphylaxis. These data demonstrate that Fc epsilon RI is necessary for the initiation of IgE-dependent anaphylactic reactions. Therefore, interfering with its function should be an effective means of treating allergy, regardless of the allergen specificity.
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Authors | D Dombrowicz, V Flamand, K K Brigman, B H Koller, J P Kinet |
Journal | Cell
(Cell)
Vol. 75
Issue 5
Pg. 969-76
(Dec 03 1993)
ISSN: 0092-8674 [Print] United States |
PMID | 8252632
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- DNA Primers
- Receptors, IgE
- Receptors, IgG
- Serotonin
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Topics |
- Anaphylaxis
(immunology)
- Animals
- B-Lymphocytes
(metabolism)
- Base Sequence
- DNA Primers
(chemistry)
- Flow Cytometry
- Mast Cells
(immunology)
- Mice
- Mice, Knockout
- Molecular Sequence Data
- Mutagenesis, Insertional
- Passive Cutaneous Anaphylaxis
(immunology)
- Receptors, IgE
(genetics, immunology, metabolism)
- Receptors, IgG
(metabolism)
- Serotonin
(metabolism)
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