Essential role for the p110δ phosphoinositide 3-kinase in the allergic response View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2004-10

AUTHORS

Khaled Ali, Antonio Bilancio, Matthew Thomas, Wayne Pearce, Alasdair M. Gilfillan, Christine Tkaczyk, Nicolas Kuehn, Alexander Gray, June Giddings, Emma Peskett, Roy Fox, Ian Bruce, Christoph Walker, Carol Sawyer, Klaus Okkenhaug, Peter Finan, Bart Vanhaesebroeck

ABSTRACT

Inflammatory substances released by mast cells induce and maintain the allergic response1,2. Mast cell differentiation and activation are regulated, respectively, by stem cell factor (SCF; also known as Kit ligand) and by allergen in complex with allergen-specific immunoglobulin E (IgE)2,3. Activated SCF receptors and high-affinity receptors for IgE (FcɛRI) engage phosphoinositide 3-kinases (PI(3)Ks) to generate intracellular lipid second messenger signals2,3,4,5. Here, we report that genetic or pharmacological inactivation of the p110δ isoform of PI(3)K in mast cells leads to defective SCF-mediated in vitro proliferation, adhesion and migration, and to impaired allergen–IgE-induced degranulation and cytokine release. Inactivation of p110δ protects mice against anaphylactic allergic responses. These results identify p110δ as a new target for therapeutic intervention in allergy and mast-cell-related pathologies. More... »

PAGES

1007-1011

Journal

TITLE

Nature

ISSUE

7011

VOLUME

431

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature02991

DOI

http://dx.doi.org/10.1038/nature02991

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1032802342

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15496927


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