Skip to main navigation Skip to search Skip to main content

Expression of the inhibitory CD200 receptor is associated with alternative macrophage activation

  • Nathalie Koning
  • , Marco Van Eijk
  • , Walter Pouwels
  • , Michael S.M. Brouwer
  • , David Voehringer
  • , Inge Huitinga
  • , Robert M. Hoek
  • , Geert Raes
  • , Jörg Hamann*
  • *Corresponding author for this work
  • Netherlands Institute for Neuroscience
  • University of Amsterdam
  • extern
  • Ludwig Maximilian University of Munich
  • Vrije Universiteit Brussel
  • Flanders Institute for Biotechnology

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Classical macrophage activation is inhibited by the CD200 receptor (CD200R). Here, we show that CD200R expression was specifically induced on human in vitro polarized macrophages of the alternatively activated M2a subtype, generated by incubation with IL-4 or IL-13. In mice, peritoneal M2 macrophages, elicited during infection with the parasites Taenia crassiceps or Trypanosoma brucei brucei, expressed increased CD200R levels compared to those derived from uninfected mice. However, in vitrostimulation of mouse peritoneal macrophages and T. crassiceps infection in IL-4-/- and IL-4R-/- mice showed that, in contrast to humans, induction of CD200R in mice was not IL-4 or IL-13 dependent. Our data identify CD200R as a suitable marker for alternatively activated macrophages in humans and corroborate observations of distinct species- and/or site-specific mechanisms regulating macrophage polarization in mouse and man.

Original languageEnglish
Pages (from-to)195-200
Number of pages6
JournalJournal of Innate Immunity
Volume2
Issue number2
DOIs
Publication statusPublished - Feb 2010
Externally publishedYes

Keywords

  • IL-4
  • Immune inhibition
  • Macrophage polarization
  • Parasite infection
  • Type 2 responses

Fingerprint

Dive into the research topics of 'Expression of the inhibitory CD200 receptor is associated with alternative macrophage activation'. Together they form a unique fingerprint.

Cite this