Adenosine signaling in T cell activation favors development of IL-17 positive cells with suppressive properties

It is assumed that the anti-inflammatory nucleoside adenosine can shape immune responses by shifting the Treg/Th17 balance in favor of Tregs. This assumption is based on in vivo and vitro studies mostly performed in murine models and warrants confirmation in human models. In the study underlying these microarray data, we demonstrate that the pan-adenosine agonist 5'-N-ethylcarboxamidoadenosine (NECA) skews human CD3+ T cell responses towards non-inflammatory Th17 cells. We used microarrays to confirm transcriptome changes consistent with genetic signatures of non-pathogenic Th17 cells and to explore relevant metabolic pathways potentially contributing to this development. CD3+ T cells collected from healthy human donors (n= 3) were stimulated with anti-CD3/anti-CD28-streptamer premix (iba Lifesciences, Göttingen) and cultured with (positive) and without (negative) the addition of 50 uM NECA for three days. Cells were then harvested and prepared for RNA extraction and hybridization on Affymetrix microarrays. Cells cultured without NECA (negative) served as reference samples.