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Suppression of IgE‐mediated allergic responses by Rgs13
Author(s) -
Bansal Geetanjali,
Xie Zhihui,
Rao Sudhir,
Nocka Karl,
Druey Kirk
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.910.1
Subject(s) - degranulation , immunoglobulin e , immunology , mast cell , microbiology and biotechnology , receptor , immune system , g protein coupled receptor , proinflammatory cytokine , allergic inflammation , chemistry , g protein , signal transduction , allergy , antibody , biology , inflammation , biochemistry
Mast cells provoke allergic responses through degranulation and release of proinflammatory mediators after antigen crosslinking of the high affinity immunoglobulin E (IgE) receptor (FcƒÕRI). Regulator of G protein Signaling (RGS) proteins negatively control G‐protein‐coupled receptor‐mediated signaling through GTPase accelerating protein (GAP) activity. Here, we show that Rgs13 inhibits allergic responses by physically interacting with the regulatory p85 alpha subunit of PI3K in mast cells and disrupting its association with an FceRI‐activated scaffold complex. Rgs13¡V/¡V mice exhibited increased IgE‐mediated mast cell degranulation and anaphylaxis. Thus, apart from its regulation of GPCRs, Rgs13 inhibits immune receptor‐induced signalosome assembly in MCs. Abnormal Rgs13 expression or function may underlie some cases of idiopathic anaphylaxis or disorders of amplified MC activity.