Regulation of macrophage function by adenosine

G. Haskó, Pál Pacher

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

Following its release into the extracellular space in response to metabolic disturbances, the endogenous nucleoside adenosine exerts a range of immunomodulatory effects and cells of the mononuclear phagocyte system are among its major targets. Adenosine governs mononuclear phagocyte functions via 4 G-protein-coupled cell membrane receptors, which are denoted A 1, A 2A, A 2B, and A 3 receptors. Adenosine promotes osteoclast differentiation via A 1 receptors and alters monocyte to dendritic cell differentiation through A 2B receptors. Adenosine downregulates classical macrophage activation mainly through A 2A receptors. In contrast A 2B receptor activation upregulates alternative macrophage activation. Adenosine promotes angiogenesis, which is mediated by inducing the production of vascular endothelial growth factor by mononuclear phagocytes through A 2A, A 2B, and A 3 receptors. By regulating mononuclear phagocyte function adenosine dictates the course of inflammatory and vascular diseases and cancer.

Original languageEnglish
Pages (from-to)865-869
Number of pages5
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume32
Issue number4
DOIs
Publication statusPublished - Apr 2012

Fingerprint

Adenosine
Macrophages
Phagocytes
Macrophage Activation
Mononuclear Phagocyte System
Extracellular Space
Osteoclasts
Vascular Diseases
Nucleosides
GTP-Binding Proteins
Dendritic Cells
Vascular Endothelial Growth Factor A
Monocytes
Cell Differentiation
Up-Regulation
Down-Regulation
Cell Membrane
Neoplasms

Keywords

  • cytokines
  • G proteins
  • immune system
  • immunosuppressive therapy
  • macrophages

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Regulation of macrophage function by adenosine. / Haskó, G.; Pacher, Pál.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 32, No. 4, 04.2012, p. 865-869.

Research output: Contribution to journalArticle

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