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

Abstract

Letter to Blood| January 5, 2023 CD39/CD73 dysregulation and adenosine metabolism contribute to T-cell immunosuppression in patients with Sézary syndrome Yuliya Yakymiv, Yuliya Yakymiv ∗ 1Laboratory of Immunogenetics, Department of Medical Sciences, University of Turin, Turin, Italy https://orcid.org/0000-0002-9598-3462 Search for other works by this author on: This Site PubMed Google Scholar Sara Marchisio, Sara Marchisio ∗ 1Laboratory of Immunogenetics, Department of Medical Sciences, University of Turin, Turin, Italy https://orcid.org/0000-0001-7005-837X Search for other works by this author on: This Site PubMed Google Scholar Erika Ortolan, Erika Ortolan 1Laboratory of Immunogenetics, Department of Medical Sciences, University of Turin, Turin, Italy https://orcid.org/0000-0003-2287-9020 Search for other works by this author on: This Site PubMed Google Scholar Cristiano Bracci, Cristiano Bracci 1Laboratory of Immunogenetics, Department of Medical Sciences, University of Turin, Turin, Italy Search for other works by this author on: This Site PubMed Google Scholar Rebecca Senetta, Rebecca Senetta 2Pathology Unit, Department of Oncology, University of Turin, Turin, Italy Search for other works by this author on: This Site PubMed Google Scholar Maria Rebecca Rumore, Maria Rebecca Rumore 2Pathology Unit, Department of Oncology, University of Turin, Turin, Italy Search for other works by this author on: This Site PubMed Google Scholar Cristian Tampieri, Cristian Tampieri 3Pathology Unit, Department of Medical Sciences, University of Turin, Turin, Italy Search for other works by this author on: This Site PubMed Google Scholar Marianna Fia, Marianna Fia 4Dermatologic Clinic, Department of Medical Sciences, University of Turin, Turin, Italy Search for other works by this author on: This Site PubMed Google Scholar Simone Ribero, Simone Ribero 4Dermatologic Clinic, Department of Medical Sciences, University of Turin, Turin, Italy Search for other works by this author on: This Site PubMed Google Scholar Ada Funaro, Ada Funaro † 1Laboratory of Immunogenetics, Department of Medical Sciences, University of Turin, Turin, Italy https://orcid.org/0000-0001-6341-1817 Search for other works by this author on: This Site PubMed Google Scholar Pietro Quaglino Pietro Quaglino † 4Dermatologic Clinic, Department of Medical Sciences, University of Turin, Turin, Italy Search for other works by this author on: This Site PubMed Google Scholar Blood (2023) 141 (1): 111–116. https://doi.org/10.1182/blood.2022017259 Article history Submitted: May 31, 2022 Accepted: August 14, 2022 Connected Content This is a related article to: CD39-CD73-adenosine effects in Sézary syndrome Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Request Permissions Cite Icon Cite Search Site Citation Yuliya Yakymiv, Sara Marchisio, Erika Ortolan, Cristiano Bracci, Rebecca Senetta, Maria Rebecca Rumore, Cristian Tampieri, Marianna Fia, Simone Ribero, Ada Funaro, Pietro Quaglino; CD39/CD73 dysregulation and adenosine metabolism contribute to T-cell immunosuppression in patients with Sézary syndrome. Blood 2023; 141 (1): 111–116. doi: https://doi.org/10.1182/blood.2022017259 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBlood Search Subjects: Immunobiology and Immunotherapy, Lymphoid Neoplasia TO THE EDITOR: Sézary syndrome (SS) is an aggressive subtype of cutaneous T-cell lymphoma, clinically presenting with erythroderma, lymphadenopathy, and atypical T cells (Sézary cells) in the skin, lymph nodes, and peripheral blood.1,2 As disease progresses, patients with SS develop 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.3 Overexpression of CD39 and/or CD73 in malignant circulating SS T cells has previously been reported.4,5 Here we follow up on our preliminary data by investigating the functional role of the CD39/CD73 ectoenzymes in generating immunosuppressive extracellular adenosine (ADO) in patients with SS.6,7 Our patient cohort consisted of 11 patients with SS (supplemental Table 1, available on the Blood website). At first encounter and at...