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Long-term remission in acute myeloid leukemia (AML) is generally not durable only being achieved in <50% of patients.1 Consequently there is a need to establish new treatments to prevent relapse. A promising approach is to augment the anti-tumor immune response in these patients; however, it is well established that overexpression of immunosuppressive molecules such as CD200 on the surface of AML cells directly suppresses the antitumor response. Nevertheless, blocking CD200:CD200R, only partially restores T-cell activity, suggesting that alternative immunosuppressive mechanisms need to be explored if the antitumor response in AML is to be optimally exploited.

The immunosuppressive ligands PD-L1 and CD200 are linked in AML T-cell immunosuppression: identification of a new immunotherapeutic synapse