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 journalArticle

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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

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Neutrophils
Tyrosine
Blood Platelets
C-Type Lectins
Respiratory Burst
Myeloid Cells
Phagocytosis
Tumor Necrosis Factor-alpha
Bone Marrow
Cytokines
Ligands
dectin 1

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

Cite this

Kerrigan, A. M., Dennehy, K. M., Mourão-Sá, D., Faro-Trindade, I., Willment, J. A., Taylor, P. R., ... Brown, G. D. (2009). CLEC-2 is a phagocytic activation receptor expressed on murine peripheral blood neutrophils. The Journal of Immunology, 182(7), 4150-4157. https://doi.org/10.4049/jimmunol.0802808

CLEC-2 is a phagocytic activation receptor expressed on murine peripheral blood neutrophils. / Kerrigan, Ann M; Dennehy, Kevin M; Mourão-Sá, Diego; Faro-Trindade, Inês; Willment, Janet A; Taylor, Philip R; Eble, Johannes A; Reis e Sousa, Caetano; Brown, Gordon D.

In: The Journal of Immunology, Vol. 182, No. 7, 01.04.2009, p. 4150-4157.

Research output: Contribution to journalArticle

Kerrigan, AM, Dennehy, KM, Mourão-Sá, D, Faro-Trindade, I, Willment, JA, Taylor, PR, Eble, JA, Reis e Sousa, C & Brown, GD 2009, 'CLEC-2 is a phagocytic activation receptor expressed on murine peripheral blood neutrophils', The Journal of Immunology, vol. 182, no. 7, pp. 4150-4157. https://doi.org/10.4049/jimmunol.0802808
Kerrigan AM, Dennehy KM, Mourão-Sá D, Faro-Trindade I, Willment JA, Taylor PR et al. CLEC-2 is a phagocytic activation receptor expressed on murine peripheral blood neutrophils. The Journal of Immunology. 2009 Apr 1;182(7):4150-4157. https://doi.org/10.4049/jimmunol.0802808
Kerrigan, Ann M ; Dennehy, Kevin M ; Mourão-Sá, Diego ; Faro-Trindade, Inês ; Willment, Janet A ; Taylor, Philip R ; Eble, Johannes A ; Reis e Sousa, Caetano ; Brown, Gordon D. / CLEC-2 is a phagocytic activation receptor expressed on murine peripheral blood neutrophils. In: The Journal of Immunology. 2009 ; Vol. 182, No. 7. pp. 4150-4157.
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AB - 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.

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