Dectin-1 activates Syk tyrosine kinase in a dynamic subset of macrophages for reactive oxygen production

DOI PDF 19 Citations
  • David M. Underhill
    From the Institute for Systems Biology, Seattle, WA; and Department of Laboratory Medicine, University of California, San Francisco.
  • Eddie Rossnagle
    From the Institute for Systems Biology, Seattle, WA; and Department of Laboratory Medicine, University of California, San Francisco.
  • Clifford A. Lowell
    From the Institute for Systems Biology, Seattle, WA; and Department of Laboratory Medicine, University of California, San Francisco.
  • Randi M. Simmons
    From the Institute for Systems Biology, Seattle, WA; and Department of Laboratory Medicine, University of California, San Francisco.

Abstract

<jats:title>Abstract</jats:title><jats:p>Dectin-1 is a lectin receptor for β-glucan that is important for innate macrophage recognition of fungi and contributes to phagocytosis, reactive oxygen production, and induction of inflammatory cytokines. The mechanisms by which Dectin-1 mediates intracellular signaling are just beginning to be defined. Spleen tyrosine kinase (Syk) is a protein tyrosine kinase that is critical for adaptive immune responses where it mediates signaling through B-cell receptors, T-cell receptors, and Fc receptors. Here we report that Dectin-1 activates Syk in macrophages and is important for Dectin-1-stimulated reactive oxygen production, but not for phagocytosis. Syk activation is restricted to a subpopulation of macrophages that is in equilibrium with cells that cannot activate the pathway. The proportion of macrophages using this signaling pathway can be modulated by cytokine treatment. Thus, Dectin-1 signaling reveals dynamic macrophage heterogeneity in inflammatory activation potential. (Blood. 2005;106:2543-2550)</jats:p>

Journal

  • Blood

    Blood 106 (7), 2543-2550, 2005-10-01

    American Society of Hematology

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