3 results on '"Guilhem Lalle"'
Search Results
2. NF-κB in Cancer Immunity: Friend or Foe?
- Author
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Guilhem Lalle, Yenkel Grinberg-Bleyer, and Julie Twardowski
- Subjects
Cell type ,medicine.medical_treatment ,Context (language use) ,Cancer immunity ,Review ,Biology ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Immune system ,Neoplasms ,medicine ,Transcriptional regulation ,Animals ,Humans ,NF-kappaB ,lcsh:QH301-705.5 ,030304 developmental biology ,Inflammation ,0303 health sciences ,Immunity ,NF-kappa B ,Cancer ,NF-κB ,General Medicine ,Immunotherapy ,medicine.disease ,3. Good health ,chemistry ,lcsh:Biology (General) ,030220 oncology & carcinogenesis ,Cancer research ,immunotherapy ,onco-immunology ,Signal Transduction - Abstract
The emergence of immunotherapies has definitely proven the tight relationship between malignant and immune cells, its impact on cancer outcome and its therapeutic potential. In this context, it is undoubtedly critical to decipher the transcriptional regulation of these complex interactions. Following early observations demonstrating the roles of NF-κB in cancer initiation and progression, a series of studies converge to establish NF-κB as a master regulator of immune responses to cancer. Importantly, NF-κB is a family of transcriptional activators and repressors that can act at different stages of cancer immunity. In this review, we provide an overview of the selective cell-intrinsic contributions of NF-κB to the distinct cell types that compose the tumor immune environment. We also propose a new view of NF-κB targeting drugs as a new class of immunotherapies for cancer.
- Published
- 2021
3. Tissue-restricted control of established central nervous system autoimmunity by TNF receptor 2–expressing Treg cells
- Author
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Cédric Auffray, Guilhem Lalle, Charlotte Pouchy, Yenkel Grinberg-Bleyer, David Sleurs, Harald Wajant, Gilles Marodon, Sylvie Grégoire, Yannis Lombardi, Bruno Lucas, Maryam Khosravi, Emilie Ronin, Gaëlle H. Martin, Noémie Chanson, Sahar Kassem, Benoît L. Salomon, Morgane Hilaire, Armanda Casrouge, Gestionnaire, Hal Sorbonne Université, Centre d'Immunologie et des Maladies Infectieuses (CIMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Développement Cancer et Thérapies Ciblées [Lyon] (LabEx DEVweCAN), Université de Lyon, Centre Léon Bérard [Lyon], University Hospital of Würzburg, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Centre d'Immunologie et de Maladies Infectieuses (CIMI), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)
- Subjects
Central Nervous System ,0301 basic medicine ,Encephalomyelitis, Autoimmune, Experimental ,Multiple Sclerosis ,T cell ,[SDV]Life Sciences [q-bio] ,TNF ,Priming (immunology) ,Inflammation ,chemical and pharmacologic phenomena ,medicine.disease_cause ,T-Lymphocytes, Regulatory ,Autoimmunity ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Bone Marrow ,medicine ,Animals ,Humans ,Receptors, Tumor Necrosis Factor, Type II ,CTLA-4 Antigen ,autoimmune diseases ,Mice, Knockout ,Autoimmune disease ,Multidisciplinary ,business.industry ,Experimental autoimmune encephalomyelitis ,FOXP3 ,hemic and immune systems ,Biological Sciences ,medicine.disease ,3. Good health ,[SDV] Life Sciences [q-bio] ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Immunology ,Tumor necrosis factor alpha ,Positive Regulatory Domain I-Binding Factor 1 ,medicine.symptom ,business ,Treg cells ,Signal Transduction - Abstract
International audience; CD4+Foxp3+ regulatory T (Treg) cells are central modulators of autoimmune diseases. However, the timing and location of Treg cell-mediated suppression of tissue-specific autoimmunity remain undefined. Here, we addressed these questions by investigating the role of tumor necrosis factor (TNF) receptor 2 (TNFR2) signaling in Treg cells during experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. We found that TNFR2-expressing Treg cells were critical to suppress EAE at peak disease in the central nervous system but had no impact on T cell priming in lymphoid tissues at disease onset. Mechanistically, TNFR2 signaling maintained functional Treg cells with sustained expression of CTLA-4 and Blimp-1, allowing active suppression of pathogenic T cells in the inflamed central nervous system. This late effect of Treg cells was further confirmed by treating mice with TNF and TNFR2 agonists and antagonists. Our findings show that endogenous Treg cells specifically suppress an autoimmune disease by acting in the target tissue during overt inflammation. Moreover, they bring a mechanistic insight to some of the adverse effects of anti-TNF therapy in patients.
- Published
- 2021
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