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Prepublished online as a Blood First Edition Paper on November 21, 2002; DOI 10.1182/blood-2002-07-2113.
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Blood, 15 May 2003, Vol. 101, No. 10, pp. 3985-3990
IMMUNOBIOLOGY
Adenosine affects expression of membrane molecules, cytokine and
chemokine release, and the T-cell stimulatory capacity of human
dendritic cells
Elisabeth Panther,
Silvia Corinti,
Marco Idzko,
Yared Herouy,
Matthias Napp,
Andrea la
Sala,
Giampiero Girolomoni, and
Johannes Norgauer
From the Department of Experimental Dermatology
and Pneumology, University of Freiburg, Germany; and the
Laboratory of Immunology, Istituto Dermopatico dell'Immacolata,
Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS),
Roma, Italy
Dendritic cells (DCs) express functional purinergic type 1 receptors, but the effects of adenosine in these antigen-presenting cells have been only marginally investigated. Here, we further characterized the biologic activity of adenosine in immature DCs (iDCs)
and lipopolysaccharide (LPS)-matured DCs (mDCs). Chronic stimulation
with adenosine enhanced the macropinocytotic activity and the membrane
expression of CD80, CD86, major histocompatibility complex
(MHC) class I, and HLA-DR molecules on iDCs. Adenosine also
increased LPS-induced CD54, CD80, MHC class I, and HLA-DR molecule
expression in mDCs. In addition, adenosine dose-dependently inhibited
tumor necrosis factor  and interleukin-12 (IL-12) release, whereas it enhanced the secretion of IL-10 from mDCs. The use of selective receptor agonists revealed that the modulation
of the cytokine and cell-surface marker profile was due to
activation of A2 adenosine receptor. Functionally,
adenosine reduced the allostimulatory capacity of iDCs, but not of
mDCs. More important, DCs matured in the presence of adenosine had a
reduced capacity to induce T helper 1 (Th1) polarization of
naive CD4+ T lymphocytes. Finally, adenosine augmented the
release of the chemokine CCL17 and inhibited CXCL10 production by mDCs.
In aggregate, the results provide initial evidence that adenosine
diminishes the capacity of DCs to initiate and amplify Th1 immune responses.
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