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cells, nalm, cell, car, spplko, sppl, fig, article, cart, glycosylation, data, loss, resistance, google, scholar, protein, binding, cas, antigen, studies, expression, nature, efficacy, supplementary, therapy, performed, antibody, analysis, cancer, clone, source, diluted, standard, min, results, function, activation, representative, experiments, fmc, med, hyperglycosylation, surface, combined, time, research, university, targeting, patients, demonstrated,

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         headline:Antigen glycosylation regulates efficacy of CAR T cells targeting CD19
         description:While chimeric antigen receptor (CAR) T cells targeting CD19 can cure a subset of patients with B cell malignancies, most patients treated will not achieve durable remission. Identification of the mechanisms leading to failure is essential to broadening the efficacy of this promising platform. Several studies have demonstrated that disruption of CD19 genes and transcripts can lead to disease relapse after initial response; however, few other tumor-intrinsic drivers of CAR T cell failure have been reported. Here we identify expression of the Golgi-resident intramembrane protease Signal peptide peptidase-like 3 (SPPL3) in malignant B cells as a potent regulator of resistance to CAR therapy. Loss of SPPL3 results in hyperglycosylation of CD19, an alteration that directly inhibits CAR T cell effector function and suppresses anti-tumor cytotoxicity. Alternatively, over-expression of SPPL3 drives loss of CD19 protein, also enabling resistance. In this pre-clinical model these findings identify post-translational modification of CD19 as a mechanism of antigen escape from CAR T cell therapy. Loss of surface CD19 expression by leukemic cells leads to resistance and relapse to CD19-targeted CAR-T therapies. Here the authors show that loss of SPPL3 in malignant B cells results in hyperglycosylation of CD19.
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      headline:Antigen glycosylation regulates efficacy of CAR T cells targeting CD19
      description:While chimeric antigen receptor (CAR) T cells targeting CD19 can cure a subset of patients with B cell malignancies, most patients treated will not achieve durable remission. Identification of the mechanisms leading to failure is essential to broadening the efficacy of this promising platform. Several studies have demonstrated that disruption of CD19 genes and transcripts can lead to disease relapse after initial response; however, few other tumor-intrinsic drivers of CAR T cell failure have been reported. Here we identify expression of the Golgi-resident intramembrane protease Signal peptide peptidase-like 3 (SPPL3) in malignant B cells as a potent regulator of resistance to CAR therapy. Loss of SPPL3 results in hyperglycosylation of CD19, an alteration that directly inhibits CAR T cell effector function and suppresses anti-tumor cytotoxicity. Alternatively, over-expression of SPPL3 drives loss of CD19 protein, also enabling resistance. In this pre-clinical model these findings identify post-translational modification of CD19 as a mechanism of antigen escape from CAR T cell therapy. Loss of surface CD19 expression by leukemic cells leads to resistance and relapse to CD19-targeted CAR-T therapies. Here the authors show that loss of SPPL3 in malignant B cells results in hyperglycosylation of CD19.
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         name:Center for Genome Integrity, Siteman Cancer Center, Washington University School of Medicine, Saint Louis, USA
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            address:
               name:Biochemistry and Molecular Biology, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany
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      name:Nathan Singh
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            address:
               name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
               type:PostalAddress
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      email:[email protected]
PostalAddress:
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Department of Pediatrics, Washington University School of Medicine, Saint Louis, USA
      name:Biochemistry and Molecular Biology, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA
      name:Biochemistry and Molecular Biology, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany
      name:Division of Hematology, Washington University School of Medicine, Saint Louis, USA
      name:Division of Hematology and Oncology, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Division of Hematology and Oncology, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Biomedical and Health Informatics, The Children’s Hospital of Philadelphia, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, The Children’s Hospital of Philadelphia, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, The Children’s Hospital of Philadelphia, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA
      name:Department of Pediatrics, Washington University School of Medicine, Saint Louis, USA
      name:Center for Genome Integrity, Siteman Cancer Center, Washington University School of Medicine, Saint Louis, USA
      name:Biochemistry and Molecular Biology, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany
      name:Division of Oncology, Washington University School of Medicine, Saint Louis, USA

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