Journal
NATURE IMMUNOLOGY
Volume 7, Issue 12, Pages 1293-1298Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1399
Keywords
-
Categories
Funding
- NCRR NIH HHS [C06-RR12538-01] Funding Source: Medline
- NIAID NIH HHS [T32 AI07407, AI18697, R01 AI018697] Funding Source: Medline
- NIGMS NIH HHS [GM64750] Funding Source: Medline
Ask authors/readers for more resources
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 5 of allergic reactions and set the stage for further studies of the involvement of ADAM10 in CD23-dependent pathologies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available