CD73 can promote adenosine production and release into the tumor microenvironment, reducing immune activity. Inhibition of CD73 may stimulate T-cell activity.
CD39 catalyzes ATP or ADP into AMP, which is then converted by CD73 to adenosine, which may mediate immunosuppressive effects on T cells.5
- In cellular studies, adenosine powerfully inhibits the antitumor immune response, including cytokine proliferation and production1
- Preclinical research has identified tumor-derived CD73 as a contributor to immune escape in cancer, and inhibition of CD73 activity can stimulate T-cell activity7
- Preclinical studies have also shown that the blockade of CD73 in combination with checkpoint inhibitors can enhance antitumor activity8
1. Kobie JJ, Shah PR, Yang L, Rebhahn JA, Fowell DJ, Mosmann TR. T regulatory and primed uncommitted CD4 T cells express CD73, which suppresses effector CD4 T cells by converting 5’-adenosine monophosphate to adenosine. J Immunol. 2006;177(10):6780-6786. 2. Deaglio S, Dwyer KM, Gao W, et al. Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression. J Exp Med. 2007;204(6):1257-1265. 3. Picher M, Burch LH, Hirsh AJ, Spychala J, Boucher RC. Ecto 5’-nucleotidase and nonspecific alkaline phosphatase. J Biol Chem. 2003;278(15):13468-13479. 4. Häusler SF, del Barrio IM, Strohschein J, et al. Ectonucleotidases CD39 and CD73 on OvCA cells are potent