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J Leukoc Biol. 2016 Feb;99(2):289-99. doi: 10.1189/jlb.1A0514-267RR. Epub 2015 Sep 17.

Purinergic signaling during macrophage differentiation results in M2 alternative activated macrophages.

Author information

1
Unidad de Inflamación Molecular y Cirugía Experimental, Centro de Investigación Biomédica en Red en el Área temática de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto Murciano de Investigación Biosanitaria, Hospital Clínico Universitario Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain.
2
Unidad de Inflamación Molecular y Cirugía Experimental, Centro de Investigación Biomédica en Red en el Área temática de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto Murciano de Investigación Biosanitaria, Hospital Clínico Universitario Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain pablo.pelegrin@ffis.es.

Abstract

Macrophages represent a highly heterogenic cell population of the innate immune system, with important roles in the initiation and resolution of the inflammatory response. Purinergic signaling regulates both M1 and M2 macrophage function at different levels by controlling the secretion of cytokines, phagocytosis, and the production of reactive oxygen species. We found that extracellular nucleotides arrest macrophage differentiation from bone marrow precursors via adenosine and P2 receptors. This results in a mature macrophage with increased expression of M2, but not M1, genes. Similar to adenosine and ATP, macrophage growth arrested with LPS treatment resulted in an increase of the M2-related marker Ym1. Recombinant Ym1 was able to affect macrophage proliferation and could, potentially, be involved in the arrest of macrophage growth during hematopoiesis.

KEYWORDS:

Ym1; adenosine; adenosine receptors; extracellular ATP; purinergic receptors

PMID:
26382298
DOI:
10.1189/jlb.1A0514-267RR
[Indexed for MEDLINE]

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