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We are analyzing https://www.nature.com/articles/s41467-020-19970-9.

Title:
Tipping the immunostimulatory and inhibitory DAMP balance to harness immunogenic cell death | Nature Communications
Description:
Induction of tumor cell death is the therapeutic goal for most anticancer drugs. Yet, a mode of drug-induced cell death, known as immunogenic cell death (ICD), can propagate antitumoral immunity to augment therapeutic efficacy. Currently, the molecular hallmark of ICD features the release of damage-associated molecular patterns (DAMPs) by dying cancer cells. Here, we show that gemcitabine, a standard chemotherapy for various solid tumors, triggers hallmark immunostimualtory DAMP release (e.g., calreticulin, HSP70, and HMGB1); however, is unable to induce ICD. Mechanistic studies reveal gemcitabine concurrently triggers prostaglandin E2 release as an inhibitory DAMP to counterpoise the adjuvanticity of immunostimulatory DAMPs. Pharmacological blockade of prostaglandin E2 biosythesis favors CD103+ dendritic cell activation that primes a Tc1-polarized CD8+ T cell response to bolster tumor rejection. Herein, we postulate that an intricate balance between immunostimulatory and inhibitory DAMPs could determine the outcome of drug-induced ICD and pose COX-2/prostaglandin E2 blockade as a strategy to harness ICD. Most chemotherapeutic agents, including gemcitabine, do not elicit immunogenic cell death, a phenomenon associated with the release of damage-associated molecule patterns (DAMPs). Here, the authors show that gemcitabine-treated dying cancer cells express hallmark DAMPs but their immunogenic properties are hindered by the concomitant release of the inhibitory DAMP PGE2.
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Keywords {🔍}

cells, cell, fig, cancer, gemcitabine, death, immunogenic, blockade, damps, tumor, release, pge, dendritic, immune, damp, response, vaccination, treatment, expression, supplementary, mice, data, icd, media, chemotherapy, biolegend, analysis, nature, bladder, hallmark, cultured, immunol, immunity, results, assay, article, protein, idamp, murine, flow, immunostimulatory, inhibitory, coxpge, crt, days, bmdcs, antitumoral, surface, panc, control,

Topics {✒️}

nature portfolio privacy policy research design granulocyte–macrophage colony-stimulating factor professional antigen-presenting cells advertising high-throughput qpcr-based platform triggers hallmark immunostimualtory damp release cox-2/pge2-blocked vaccine groups nature https type-1-polarized cd103+ dc/cd8+ reprints nature cox-2/pge2 blockade exhibited drug-induced cell death mass spectrometry-based assays helper t-cell response cedars-sinai medical center hsp heat-shock protein cell death-induced release vaccine-draining lymph nodes tc1-polarized immune response t-cell polarizing effects heat-shock protein 70 kda u-bottom plates coated bona fide icd-inducers17 fluorescence-activated cell sorting low-dose oral cyclophosphamide kaplan–meier survival analysis full size image bona fide icd-vaccine cancer cells pre-treated author information authors g69 bladder cancer model cytometry/cell sorting cores batf3 deficiency reveals l-arginine metabolism antitumoral tc1-polarized immunity cox-2/pge2-blockade groups 1x insulin-transferrin-selenium hallmark antigen-receptor clec9a44 chemotherapy-induced damp release dendritic cell pd-l1 cox-2/pge2-blockade arm live/dead-nearir stain host-derived “danger” signals gemctx-treated cd103+ bmdcs bona fide icd-inducers cyclooxygenase-dependent tumor growth cell expansion/memory formation54

Questions {❓}

  • Immunological decision-making: how does the immune system decide to mount a helper T-cell response?

Schema {🗺️}

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      description:Induction of tumor cell death is the therapeutic goal for most anticancer drugs. Yet, a mode of drug-induced cell death, known as immunogenic cell death (ICD), can propagate antitumoral immunity to augment therapeutic efficacy. Currently, the molecular hallmark of ICD features the release of damage-associated molecular patterns (DAMPs) by dying cancer cells. Here, we show that gemcitabine, a standard chemotherapy for various solid tumors, triggers hallmark immunostimualtory DAMP release (e.g., calreticulin, HSP70, and HMGB1); however, is unable to induce ICD. Mechanistic studies reveal gemcitabine concurrently triggers prostaglandin E2 release as an inhibitory DAMP to counterpoise the adjuvanticity of immunostimulatory DAMPs. Pharmacological blockade of prostaglandin E2 biosythesis favors CD103+ dendritic cell activation that primes a Tc1-polarized CD8+ T cell response to bolster tumor rejection. Herein, we postulate that an intricate balance between immunostimulatory and inhibitory DAMPs could determine the outcome of drug-induced ICD and pose COX-2/prostaglandin E2 blockade as a strategy to harness ICD. Most chemotherapeutic agents, including gemcitabine, do not elicit immunogenic cell death, a phenomenon associated with the release of damage-associated molecule patterns (DAMPs). Here, the authors show that gemcitabine-treated dying cancer cells express hallmark DAMPs but their immunogenic properties are hindered by the concomitant release of the inhibitory DAMP PGE2.
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            name:Baylor College of Medicine
            address:
               name:Alkek Center for Molecular Discovery, Proteomics Core, Baylor College of Medicine, Houston, USA
               type:PostalAddress
            type:Organization
      name:E. Tsouko
      affiliation:
            name:Baylor College of Medicine
            address:
               name:Department of Orthopedic Surgery, Baylor College of Medicine, Houston, USA
               type:PostalAddress
            type:Organization
      name:H. Gao
      affiliation:
            name:Cedars-Sinai Medical Center
            address:
               name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
               type:PostalAddress
            type:Organization
      name:A. Kasabyan
      affiliation:
            name:Cedars-Sinai Medical Center
            address:
               name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
               type:PostalAddress
            type:Organization
      name:H. E. Leung
      affiliation:
            name:Baylor College of Medicine
            address:
               name:Alkek Center for Molecular Discovery, Proteomics Core, Baylor College of Medicine, Houston, USA
               type:PostalAddress
            type:Organization
      name:A. Osipov
      affiliation:
            name:Cedars-Sinai Medical Center
            address:
               name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
               type:PostalAddress
            type:Organization
      name:S. Y. Jung
      url:http://orcid.org/0000-0003-1521-7977
      affiliation:
            name:Baylor College of Medicine
            address:
               name:Alkek Center for Molecular Discovery, Proteomics Core, Baylor College of Medicine, Houston, USA
               type:PostalAddress
            type:Organization
      name:A. V. Kurtova
      affiliation:
            name:Baylor College of Medicine
            address:
               name:Graduate Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, USA
               type:PostalAddress
            type:Organization
      name:K. S. Chan
      affiliation:
            name:Cedars-Sinai Medical Center
            address:
               name:Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, USA
               type:PostalAddress
            type:Organization
            name:Cedars-Sinai Medical Center
            address:
               name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Graduate Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, USA
      name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Graduate Institute of Medical Sciences, Taipei Medical University, Taipei City, Taiwan
      name:Alkek Center for Molecular Discovery, Proteomics Core, Baylor College of Medicine, Houston, USA
      name:Department of Orthopedic Surgery, Baylor College of Medicine, Houston, USA
      name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Alkek Center for Molecular Discovery, Proteomics Core, Baylor College of Medicine, Houston, USA
      name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Alkek Center for Molecular Discovery, Proteomics Core, Baylor College of Medicine, Houston, USA
      name:Graduate Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, USA
      name:Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, USA
      name:Samuel Oschin Cancer Center, Cedars-Sinai Medical Center, Los Angeles, USA

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