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* Institute of Interdisciplinary Research, School of Medicine, Departments of
Immunology and
Medical Chemistry, Erasme Hospital, Université Libre de Brussels, Brussels, Belgium
ATP has been reported to inhibit or stimulate lymphoid cell
proliferation, depending on the origin of the cells. Agents that
increase cAMP, such as PGE2, inhibit human CD4+
T cell activation. We demonstrate that several ATP derivatives increase
cAMP in both freshly purified and activated human peripheral blood
CD4+ T cells. The rank order of potency of the various
nucleotides was: adenosine 5'-O-(3-thiotriphosphate)
(ATP
S) 
2'- and 3'-O-(4-benzoylbenzoyl) ATP
(BzATP) > ATP > 2-methylthio-ATP >> dATP,
2-propylthio-
,-dichloromethylene-D-ATP, UDP, UTP.
This effect did not involve the activation of A2Rs by
adenosine or the synthesis of prostaglandins. ATPS had no effect on
cytosolic calcium, whereas BzATP induced an influx of extracellular
calcium. ATPS and BzATP inhibited secretion of IL-2, IL-5, IL-10,
and IFN-; expression of CD25; and proliferation after activation of
CD4+ T cells by immobilized anti-CD3 and soluble
anti-CD28 Abs, without increasing cell death. Taken together, our
results suggest that extracellular adenine nucleotides inhibit
CD4+ T cell activation via an increase in cAMP mediated by
an unidentified P2YR, which might thus constitute a new therapeutic
target in immunosuppressive treatments.
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