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Up-Regulates the A2B Adenosine Receptor Expression in Macrophages: A Mechanism of Macrophage Deactivation1
*
Departament de Fisiologia (Group of Macrophage), Facultat de Biologia, and Fundació August Pi i Sunyer, Campus Bellvitge, Barcelona, Spain; and
Departament de Bioquímica i Biologia Molecular, Facultat de Química, Universitat de Barcelona, Barcelona, Spain
Adenosine is a potent endogenous anti-inflammatory agent
released by cells in metabolically unfavorable conditions, such as
hypoxia or ischemia. Adenosine modulates different functional
activities in macrophages. Some of these activities are believed to be
induced through the uptake of adenosine into the macrophages, while
others are due to the interaction with specific cell surface receptors.
In murine bone marrow-derived macrophages, the use of different
radioligands for adenosine receptors suggests the presence of
A2B and A3 adenosine receptor subtypes. The
presence of A2B receptors was confirmed by flow cytometry
using specific Abs. The A2B receptor is functional in
murine macrophages, as indicated by the fact that agonists of
A2B receptors, but not agonists for A1,
A2A, or A3, lead to an increase in cAMP levels.
IFN-
up-regulates the surface protein and gene expression of the
A2B adenosine receptor by induction of de novo synthesis.
The up-regulation of A2B receptors correlates with an
increase in cAMP production in macrophages treated with adenosine
receptor agonist. The stimulation of A2B receptors by
adenosine or its analogues inhibits the IFN--induced expression of
MHC class II genes and also the IFN--induced expression of nitric
oxide synthase and of proinflammatory cytokines. Therefore, the
up-regulation of the A2B adenosine receptor expression
induced by IFN- could be a feedback mechanism for macrophage
deactivation.
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