CLEC-2 is a phagocytic activation receptor expressed on murine peripheral blood neutrophils

Ann M Kerrigan, Kevin M Dennehy, Diego Mourão-Sá, Inês Faro-Trindade, Janet A Willment, Philip R Taylor, Johannes A Eble, Caetano Reis e Sousa, Gordon D Brown

Research output: Contribution to journalArticlepeer-review

104 Citations (Scopus)

Abstract

CLEC-2 is a member of the "dectin-1 cluster" of C-type lectin-like receptors and was originally thought to be restricted to platelets. In this study, we demonstrate that murine CLEC-2 is also expressed by peripheral blood neutrophils, but only weakly by bone marrow or elicited inflammatory neutrophils. On circulating neutrophils, CLEC-2 can mediate phagocytosis of Ab-coated beads and the production of proinflammatory cytokines, including TNF-alpha, in response to the CLEC-2 ligand, rhodocytin. CLEC-2 possesses a tyrosine-based cytoplasmic motif similar to that of dectin-1, and we show using chimeric analyses that the activities of this receptor are dependent on this tyrosine. Like dectin-1, CLEC-2 can recruit the signaling kinase Syk in myeloid cells, however, stimulation of this pathway does not induce the respiratory burst. These data therefore demonstrate that CLEC-2 expression is not restricted to platelets and that it functions as an activation receptor on neutrophils.
Original languageEnglish
Pages (from-to)4150-4157
Number of pages8
JournalThe Journal of Immunology
Volume182
Issue number7
DOIs
Publication statusPublished - 1 Apr 2009

Keywords

  • animals
  • blotting, western
  • enzyme-linked immunosorbent assay
  • flow cytometry
  • gene expression
  • gene expression regulation
  • immunoprecipitation
  • intracellular signaling peptides and proteins
  • lectins, C-type
  • mice
  • neutrophils
  • phagocytosis
  • protein-tyrosine kinases
  • respiratory burst
  • tumor necrosis factor-alpha

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