Dectin-2 is predominantly myeloid restricted and exhibits unique activation-dependent expression on maturing inflammatory monocytes elicited in vivo

P. R. Taylor, D. M. Reid, S. E. Heinsbroek, G. D. Brown, S. Gordon, Simon Yuk Chun Wong

Research output: Contribution to journalArticlepeer-review

111 Citations (Scopus)

Abstract

Dectin-2 is a recently described dendritic-cell-associated receptor, suggested to be involved in the initiation and maintenance of UV-induced tolerance. To understand the physiological relevance of the proposed functions of this C-type lectin-like receptor, we have generated monoclonal antibodies against its extracellular domain and performed a detailed study of its expression. In naive mice, Dectin-2 has a novel distribution pattern compared with other myeloid markers, but is predominantly expressed by a wide variety of tissue macrophages. Its expression was limited on dendritic cells and notably absent from brain microglia and choroid plexus or meningeal macrophages. On peripheral blood monocytes, Dectin-2 expression was very low on the surface but was transiently and markedly up-regulated on induction of inflammation in vivo using a variety of stimuli. This change in Dectin-2 expression occurs on 'inflammatory' monocytes after arrival at the inflammatory lesion as demonstrated by adoptive cell-transfer studies, and is independent of whether the macrophages elicited by the stimuli ultimately expressed Dectin-2. These observations show Dectin-2 expression to be characteristic of monocyte activation/maturation at an inflammatory lesion and provide a new perspective on the interpretation of Dectin-2 function in vivo.

Original languageEnglish
Pages (from-to)2163-2174
Number of pages11
JournalEuropean Journal of Immunology
Volume35
Issue number7
DOIs
Publication statusPublished - Jul 2005

Keywords

  • macrophage
  • lectin
  • inflammation
  • monocyte
  • BETA-GLUCAN RECEPTOR
  • MONOCLONAL-ANTIBODY
  • MOUSE MACROPHAGE
  • DC-SIGN
  • RECOGNITION
  • CELLS
  • IDENTIFICATION
  • GENE
  • PROTEIN
  • CLONING

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