Sergey Apasov

TL;DR: Although using the hypoxia→adenosine→A2AR pathway inhibitors may improve antitumor immunity, the recruitment of this pathway by selective drugs is expected to attenuate the autoimmune tissue damage.

TL;DR: A2A receptor-triggered generation of intracellular cAMP inhibits activated immune cells in a delayed negative feedback manner to prevent additional tissue damage, and targeting A2A adenosine receptors may have important clinical applications.

TL;DR: The possible role of adenosine receptors in the regulation of lymphocyte expansion is suggested and the downregulation of A2a purinergic receptors on T cells as a potentially attractive pharmacologic target is pointed to.

TL;DR: The ambient 20% oxygen tension (plus 2-ME) is remarkably well suited for immunologic specificity and cytotoxicity studies, but oxygen dependence should be taken into account during the design and interpretation of results of in vitro T cell development assays and gene expression studies in vivo.

TL;DR: The demonstration of cross-talk between the A2A receptors and TCR in both directions support the possible role of A 2A receptors in mechanisms of extAdo-mediated immunosuppression in vivounder adenosine deaminase deficiency and hypoxic conditions in, e.g., solid tumors.