Abstract |
CD23, the low-affinity immunoglobulin E receptor, is an important modulator of the allergic response and of diseases such as rheumatoid arthritis. The proteolytic release of CD23 from cells is considered a key event in the allergic response. Here we used loss-of-function and gain-of-function experiments with cells lacking or overexpressing candidate CD23-releasing enzymes (ADAM8, ADAM9, ADAM10, ADAM12, ADAM15, ADAM17, ADAM19 and ADAM33), ADAM-knockout mice and a selective inhibitor to identify ADAM10 as the main CD23-releasing enzyme in vivo. Our findings provide a likely target for the treatment of allergic reactions and set the stage for further studies of the involvement of ADAM10 in CD23-dependent pathologies.
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Authors | Gisela Weskamp, Jill W Ford, Jamie Sturgill, Steve Martin, Andrew J P Docherty, Steven Swendeman, Neil Broadway, Dieter Hartmann, Paul Saftig, Shelby Umland, Atsuko Sehara-Fujisawa, Roy A Black, Andreas Ludwig, J David Becherer, Daniel H Conrad, Carl P Blobel |
Journal | Nature immunology
(Nat Immunol)
Vol. 7
Issue 12
Pg. 1293-8
(Dec 2006)
ISSN: 1529-2908 [Print] United States |
PMID | 17072319
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Membrane Proteins
- Receptors, IgE
- Amyloid Precursor Protein Secretases
- ADAM Proteins
- ADAM10 Protein
- Adam10 protein, mouse
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Topics |
- ADAM Proteins
(immunology, metabolism)
- ADAM10 Protein
- Amyloid Precursor Protein Secretases
(immunology, metabolism)
- Animals
- B-Lymphocytes
(immunology, metabolism)
- Electrophoresis, Polyacrylamide Gel
- Enzyme-Linked Immunosorbent Assay
- Fibroblasts
(immunology, metabolism)
- Flow Cytometry
- Humans
- Immunoblotting
- Membrane Proteins
(immunology, metabolism)
- Mice
- Mice, Knockout
- Receptors, IgE
(immunology, metabolism)
- Transfection
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