Murine B Cells Regulate Serum IgE Levels in a CD23-Dependent Manner

Department of Pediatrics, University of California, San Francisco, San Francisco, CA 94143, USA.
The Journal of Immunology (Impact Factor: 4.92). 11/2010; 185(9):5040-7. DOI: 10.4049/jimmunol.1001900
Source: PubMed


The manifestations of allergic disorders are closely tied to the biologic effects of IgE activation with Ag. In immediate hypersensitivity reactions, IgE effector function requires prior binding to innate immune cells, primarily mast cells and basophils, with the blood acting as a reservoir for unbound IgE. As the severity of allergic disease is proportional to the size of this unbound IgE pool, we hypothesized that cellular mechanisms exist to limit the size and/or enhance the clearance of free IgE molecules. We examined this in mice by engineering a reporter IgE molecule that allowed us to track the fate of IgE molecules in vivo. The absence of FcεRI-expressing cells did not affect serum IgE levels, but B cells regulated serum IgE by controlling the size of the free IgE pool. B cells captured IgE by direct binding to the low-affinity IgE receptor, CD23. These data indicate a mechanism regulating serum IgE and additionally clarify the role of CD23 in this process.

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Available from: Laurence E. Cheng, Feb 05, 2014
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    • "CD23 is the low-affinity receptor for IgE and has been implicated in a number of inflammatory conditions, and is considered to be important in the regulation of IgE production . An altered expression of CD23 has been widely associated with allergic diseases (Morris et al., 1994; Rosenwasser and Meng, 2005; Cheng et al., 2010). Based on these notions, we found that lung CD23 expression was significantly increased in S1P-treated compared with vehicle mice. "
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