ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23

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

doi:10.1038/ni1399

ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23

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

Research output: Contribution to journal › Article › peer-review

186 Scopus citations

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.

Original language	English
Pages (from-to)	1293-1298
Number of pages	6
Journal	Nature Immunology
Volume	7
Issue number	12
DOIs	https://doi.org/10.1038/ni1399
State	Published - Dec 2006

Bibliographical note

Funding Information:
We thank V. Nikolenko and A. Shirazi for technical assistance; recombinant mouse IL-4 was a gift from W. Paul (US National Institutes of Health). Supported by the US National Institutes of Health (GM64750 to C.P.B and AI18697 to D.H.C.), the US National Institute of Allergy and Infectious Diseases (T32 AI07407 to J.W.F.) and the National Institutes of Health National Center for Research Resources Research Facilities Improvement Program (C06-RR12538-01 for construction of the facility housing the laboratory of C.P.B.).

Funding

We thank V. Nikolenko and A. Shirazi for technical assistance; recombinant mouse IL-4 was a gift from W. Paul (US National Institutes of Health). Supported by the US National Institutes of Health (GM64750 to C.P.B and AI18697 to D.H.C.), the US National Institute of Allergy and Infectious Diseases (T32 AI07407 to J.W.F.) and the National Institutes of Health National Center for Research Resources Research Facilities Improvement Program (C06-RR12538-01 for construction of the facility housing the laboratory of C.P.B.).

Funders	Funder number
National Institutes of Health National Center for Research Resources Research Facilities Improvement Program	C06-RR12538-01
US National Institutes of Health/NHGRI	GM64750
National Institute of Allergy and Infectious Diseases	R01AI018697, T32 AI07407

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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10.1038/ni1399

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Weskamp, G., Ford, J. W., Sturgill, J., Martin, S., Docherty, A. J. P., Swendeman, S., Broadway, N., Hartmann, D., Saftig, P., Umland, S., Sehara-Fujisawa, A., Black, R. A., Ludwig, A., Becherer, J. D., Conrad, D. H., & Blobel, C. P. (2006). ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23. Nature Immunology, 7(12), 1293-1298. https://doi.org/10.1038/ni1399

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title = "ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23",

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.",

author = "Gisela Weskamp and Ford, {Jill W.} and Jamie Sturgill and Steve Martin and Docherty, {Andrew J.P.} and Steven Swendeman and Neil Broadway and Dieter Hartmann and Paul Saftig and Shelby Umland and Atsuko Sehara-Fujisawa and Black, {Roy A.} and Andreas Ludwig and Becherer, {J. David} and Conrad, {Daniel H.} and Blobel, {Carl P.}",

note = "Funding Information: We thank V. Nikolenko and A. Shirazi for technical assistance; recombinant mouse IL-4 was a gift from W. Paul (US National Institutes of Health). Supported by the US National Institutes of Health (GM64750 to C.P.B and AI18697 to D.H.C.), the US National Institute of Allergy and Infectious Diseases (T32 AI07407 to J.W.F.) and the National Institutes of Health National Center for Research Resources Research Facilities Improvement Program (C06-RR12538-01 for construction of the facility housing the laboratory of C.P.B.).",

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doi = "10.1038/ni1399",

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Weskamp, G, Ford, JW, Sturgill, J, Martin, S, Docherty, AJP, Swendeman, S, Broadway, N, Hartmann, D, Saftig, P, Umland, S, Sehara-Fujisawa, A, Black, RA, Ludwig, A, Becherer, JD, Conrad, DH & Blobel, CP 2006, 'ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23', Nature Immunology, vol. 7, no. 12, pp. 1293-1298. https://doi.org/10.1038/ni1399

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AU - Weskamp, Gisela

AU - Ford, Jill W.

AU - Sturgill, Jamie

AU - Martin, Steve

AU - Docherty, Andrew J.P.

AU - Swendeman, Steven

AU - Broadway, Neil

AU - Hartmann, Dieter

AU - Saftig, Paul

AU - Umland, Shelby

AU - Sehara-Fujisawa, Atsuko

AU - Black, Roy A.

AU - Ludwig, Andreas

AU - Becherer, J. David

AU - Conrad, Daniel H.

AU - Blobel, Carl P.

N1 - Funding Information: We thank V. Nikolenko and A. Shirazi for technical assistance; recombinant mouse IL-4 was a gift from W. Paul (US National Institutes of Health). Supported by the US National Institutes of Health (GM64750 to C.P.B and AI18697 to D.H.C.), the US National Institute of Allergy and Infectious Diseases (T32 AI07407 to J.W.F.) and the National Institutes of Health National Center for Research Resources Research Facilities Improvement Program (C06-RR12538-01 for construction of the facility housing the laboratory of C.P.B.).

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N2 - 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.

AB - 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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ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23

Abstract

Bibliographical note

Funding

ASJC Scopus subject areas

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