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Adenosine is an endogenously released purine nucleoside that signals through four widely expressed G protein-coupled receptors: A1, A2 A , A2 B , and A3. Of these, A 2A R is recognized as mediating major adenosine anti-inflammatory activity. During cutaneous leishmaniasis, adenosine induces immunosuppression, which promotes the establishment of infection. Herein, we demonstrated that A 2A R signaling is exploited by  Leishmania infantum  parasites, the etiologic agent that causes Visceral Leishmaniasis, to successfully colonize the vertebrate host. A 2A R gene-deleted mice exhibited a well-developed cellular reaction with a strong Th1 immune response in the parasitized organs. An intense infiltration of activated neutrophils into the disease-target organs was observed in A 2A R −/−  mice. These cells were characterized by high expression of CXCR2 and CD69 on their cell surfaces and increased  cxcl1  expression. Interestingly, this phenotype was mediated by IFN-γ on the basis that a neutralizing antibody specific to this cytokine prevented neutrophilic influx into parasitized organs. In evaluating the immunosuppressive effects, we identified a decreased number of CD4 +  FOXP3 +  T cells and reduced  il10  expression in A 2A R −/−  infected mice. During  ex vivo  cell culture, A 2A R −/−  splenocytes produced smaller amounts of IL-10. In conclusion, we demonstrated that the A 2A R signaling pathway is detrimental to development of Th1-type adaptive immunity and that this pathway could be associated with the regulatory process. In particular, it promotes parasite surveillance.

Leishmania infantum Parasites Subvert the Host Inflammatory Response through the Adenosine A2A Receptor to Promote the Establishment of Infection