Adenosine and cAMP signalling skew human dendritic cell differentiation towards a tolerogenic phenotype with defective CD8+ T-cell priming capacity

摘要: Multiple endogenous mechanisms that regulate immune and inflammatory processes contribute to the maintenance of peripheral tolerance prevent chronic inflammation in mammals. Yet pathogens tumours are able exploit these homeostatic pathways foster immunosuppressive microenvironments evade surveillance. The release adenosine extracellular space contributes phenomena by exerting a broad range immunomodulatory effects. Here we document influence receptor triggering on human dendritic cell differentiation functions. We show expression several proteins myeloid/monocytic lineage markers was affected receptors cAMP pathway. These changes were reminiscent phenotype associated with tolerogenic cells and, functionally, translated into defective capacity prime CD8+ T-cells common tumour antigen vitro. results establish novel mechanism which hampers T-cell immunity via may as well establishment relevant biology.