| First Author | Young A | Year | 2016 |
| Journal | Cancer Cell | Volume | 30 |
| Issue | 3 | Pages | 391-403 |
| PubMed ID | 27622332 | Mgi Jnum | J:234977 |
| Mgi Id | MGI:5792584 | Doi | 10.1016/j.ccell.2016.06.025 |
| Citation | Young A, et al. (2016) Co-inhibition of CD73 and A2AR Adenosine Signaling Improves Anti-tumor Immune Responses. Cancer Cell 30(3):391-403 |
| abstractText | Preclinical studies targeting the adenosinergic pathway have gained much attention for their clinical potential in overcoming tumor-induced immunosuppression. Here, we have identified that co-blockade of the ectonucleotidase that generates adenosine CD73 and the A2A adenosine receptor (A2AR) that mediates adenosine signaling in leuokocytes, by using compound gene-targeted mice or therapeutics that target these molecules, limits tumor initiation, growth, and metastasis. This tumor control requires effector lymphocytes and interferon-gamma, while antibodies targeting CD73 promote an optimal therapeutic response in vivo when engaging activating Fc receptors. In a two-way mixed leukocyte reaction using a fully human anti-CD73, we demonstrated that Fc receptor binding augmented the production of proinflammatory cytokines. |
