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CLUSTERING OF ADENOSINE A 2B RECEPTORS WITH ECTONUCLEOTIDASES IN CAVEOLIN-RICH LIPID RAFTS UNDERLIES IMMUNOMODULATION BY LEISHMANIA AMAZONENSIS
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Extracellular adenosine plays important roles in modulating the immune responses.
We have previously demonstrated that infection of dendritic cells (DC) by Leishmania
amazonensis leads to increased expression of CD39 and CD73 and to the selective
activation of the low affinity A 2B receptors (A 2BR), which contributes to DC inhibi-
tion, without involvement of the high affinity A2AR. To understand this apparent
paradox, we now characterized the alterations of both adenosine receptors in infected
cells. With this aim, bone marrow- derived DC from C57BL/6J mice were infected
with metacyclic promastigotes of L. amazonensis. Fluorescence microscopy revealed
that L. amazonensis infection stimulates the recruitment of A2BR, but not of A2AR, to
the surface of infected DC, without altering the amount of mRNA or the total A 2BR
density, an effect dependent on lipophosphoglycan (LPG). Log- phase promastigotes
or axenic amastigotes of L. amazonensis do not stimulate A 2BR recruitment. A 2BR
clusters are localized in caveolin- rich lipid rafts and the disruption of these mem-
brane domains impairs A 2BR recruitment and activation. More importantly, our re-
sults show that A2BR co-localize with CD39 and CD73 forming a “purinergic cluster"
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