0000000001051042

AUTHOR

Joachim L. Schultze

showing 3 related works from this author

Cancer cell–autonomous contribution of type I interferon signaling to the efficacy of chemotherapy

2014

International audience; The immune system is routinely confronted with cell death resulting from the physiological turnover of renewable tissues, as well as from pathological insults of several types. We hypothesize the existence of a mechanism that allows the immune system to discriminate between physiological and pathological instances of cell death, but the factors that determine whether cellular demise is perceived as a neutral, tolerogenic or immunogenic event remain unclear 1. Infectious insults are accompanied by so-called microbe-associated molecular patterns (MAMPs), i.e., viral or bacterial products that activate immune cells through a panel of pattern-recognition receptors (PRRs)…

Myxovirus Resistance ProteinsMessengerReceptor Interferon alpha-betaInbred C57BLchemotherapyInterferon alpha-betaMiceInterferonReceptorsAnthracyclinesNeoplasm MetastasisRIG-IPattern recognition receptorAdaptor ProteinsGeneral MedicineNeoadjuvant Therapy3. Good healthGene Expression Regulation NeoplasticTreatment OutcomeReceptors Pattern RecognitionInterferon Type I[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleImmunocompetencemedicine.drugReceptorSignal TransductionBreast Neoplasms[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPattern RecognitionSettore BIO/09General Biochemistry Genetics and Molecular BiologyParacrine signallingImmune systemmedicineCXCL10AnimalsHumanscancerRNA MessengerAutocrine signallingNeoplastic[SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/ImmunotherapyToll-Like Receptor 3Mice Inbred C57BLVesicular TransportChemokine CXCL10Adaptor Proteins Vesicular TransportGene Expression RegulationDoxorubicinImmunologyTLR3RNAAdaptor Proteins Vesicular Transport; Animals; Anthracyclines; Breast Neoplasms; Chemokine CXCL10; Doxorubicin; Female; Gene Expression Regulation Neoplastic; Humans; Immunocompetence; Interferon Type I; Mice Inbred C57BL; Myxovirus Resistance Proteins; Neoadjuvant Therapy; Neoplasm Metastasis; RNA; RNA Messenger; Receptor Interferon alpha-beta; Receptors Pattern Recognition; Toll-Like Receptor 3; Treatment Outcome; Signal Transduction
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Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1.

2015

How dying tumor cells get noticed Besides killing tumor cells directly, some chemotherapies, such as anthracyclines, also activate the immune system to kill tumors. Vacchelli et al. discovered that in mice, anthracycline-induced antitumor immunity requires immune cells to express the protein formyl peptide receptor 1 (FPR1). Dendritic cells (DCs) near tumors expressed especially high amounts of FPR1. DCs normally capture fragments of dying tumor cells and use them to activate nearby T cells to kill tumors, but DCs lacking FPR1 failed to do this effectively. Individuals with breast or colon cancer expressing a variant of FPR1 and treated with anthracyclines showed poor metastasis-free and ov…

AnthracyclineColorectal cancermedicine.medical_treatmentT-LymphocytesBreast Neoplasmsmicrofluidic chipchemotherapyPolymorphism Single NucleotideFormyl peptide receptor 1immune responseMiceImmune systemImmunityCell Line TumorNeoplasmsmedicineLeukocytesAnimalsHumansAnthracyclinesAllelesAnnexin A1ChemotherapyMultidisciplinarybusiness.industryDendritic Cellsmedicine.diseaseReceptors Formyl PeptideImmunity InnateChemotherapy AdjuvantCancer cellImmunologyCancer researchFemalebusinessColorectal NeoplasmsAdjuvantFPR1 microfluidicScience (New York, N.Y.)
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Enzymatic Activity of HPGD in Treg Cells Suppresses Tconv Cells to Maintain Adipose Tissue Homeostasis and Prevent Metabolic Dysfunction.

2019

Summary Regulatory T cells (Treg cells) are important for preventing autoimmunity and maintaining tissue homeostasis, but whether Treg cells can adopt tissue- or immune-context-specific suppressive mechanisms is unclear. Here, we found that the enzyme hydroxyprostaglandin dehydrogenase (HPGD), which catabolizes prostaglandin E2 (PGE2) into the metabolite 15-keto PGE2, was highly expressed in Treg cells, particularly those in visceral adipose tissue (VAT). Nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ)-induced HPGD expression in VAT Treg cells, and consequential Treg-cell-mediated generation of 15-keto PGE2 suppressed conventional T cell activation and proliferation. C…

0301 basic medicineanalogs & derivatives [Dinoprostone]Malemetabolism [Diabetes Mellitus Type 2]Adipose tissueLymphocyte Activation15-ketoprostaglandin E2T-Lymphocytes RegulatoryJurkat cellsJurkat CellsMice0302 clinical medicineimmunology [Lymphocyte Activation]genetics [Insulin Resistance]STAT5 Transcription FactorHomeostasisImmunology and AllergyTissue homeostasisgenetics [Hydroxyprostaglandin Dehydrogenases]Mice Knockoutcytology [Intra-Abdominal Fat]enzymology [T-Lymphocytes Regulatory]FOXP3hemic and immune systems3T3 CellsCell biologyInfectious Diseases030220 oncology & carcinogenesisHydroxyprostaglandin Dehydrogenasesmedicine.symptomimmunology [T-Lymphocytes Regulatory]metabolism [STAT5 Transcription Factor]Immunologymetabolism [Dinoprostone]chemical and pharmacologic phenomenaInflammationIntra-Abdominal FatBiologyDinoprostoneCell Line03 medical and health sciencesmetabolism [Hydroxyprostaglandin Dehydrogenases]immunology [Homeostasis]medicineAnimalsHumansddc:610immunology [Intra-Abdominal Fat]HEK 293 cells030104 developmental biologyHEK293 CellsDiabetes Mellitus Type 2Cell cultureInsulin ResistanceHomeostasis
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