Regulation of tyrosine kinase activation and granule release through beta-arrestin by CXCRI

Nat Immunol. 2000 Sep;1(3):227-33. doi: 10.1038/79767.

J Barlic ¹, J D Andrews, A A Kelvin, S E Bosinger, M E DeVries, L Xu, T Dobransky, R D Feldman, S S Ferguson, D J Kelvin

Affiliations

Affiliation

1 Laboratory of Molecular Immunology and Inflammation, John P. Robarts Research Institute, 1400 Western Road, London, Ontario, Canada, N6G 2V4.

PMID: 10973280 DOI: 10.1038/79767

Abstract

Chemoattractant-stimulated granule release from neutrophils, basophils and eosinophils is critical for the innate immune response against infectious bacteria. Interleukin 8 (IL-8) activation of the Chemokine Receptor CXCRI was found to stimulate rapid formation of beta-arrestin complexes with Hck or c-Fgr. Formation of beta-arrestin-Hck complexes led to Hck activation and trafficking of the complexes to granule-rich regions. Granulocytes expressing a dominant-negative beta-arrestin-mutant did not release granules or activate tyrosine kinases after IL-8 stimulation. Thus, beta-arrestins regulate chemokine-induced granule exocytosis, indicating a broader role for beta-arrestins in the regulation of cellular functions than was previously suspected.

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