CD39/CD73 dysregulation and adenosine metabolism contribute to T cell immunosuppression in patients with Sézary syndrome

Sézary syndrome (SS) is an aggressive subtype of cutaneous T-cell lymphoma, clinically presenting with erythroderma, lymphadenopathy and atypical T cells (Sezary cells) in the skin, lymph nodes and peripheral blood. As disease progresses, SS patients present severe immunodeficiency orchestrated by tumor cells and the tumor microenvironment (TME). This immunodeficiency is worsened by therapy and is responsible for a high incidence of life-threatening infections. Overexpression of CD39 and/or CD73 in malignant circulating SS T cells has previously been reported. Here we follow on our preliminary data investigating the functional role of the CD39/CD73 ectoenzymes in generating immunosuppressive extracellular adenosine (ADO) in SS patients6,7