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Статті в журналах з теми "Inhibiteurs de points de contrôle immunitaire":
Bonnefoy, Nathalie, Daniel Olive, and Bernard Vanhove. "Les futures générations d’anticorps modulateurs des points de contrôle de la réponse immunitaire." médecine/sciences 35, no. 12 (December 2019): 966–74. http://dx.doi.org/10.1051/medsci/2019193.
Dubois, Manon, Camille Ardin, Fanny André, Arnaud Scherpereel, and Laurent Mortier. "L’immunothérapie, une révolution en oncologie." médecine/sciences 35, no. 12 (December 2019): 946–48. http://dx.doi.org/10.1051/medsci/2019226.
Chiossone, Laura, and Eric Vivier. "Nouvelles frontières de la lutte contre le cancer." Biologie Aujourd'hui 212, no. 3-4 (2018): 61–67. http://dx.doi.org/10.1051/jbio/2019011.
Kostine, Marie, Aurélien Marabelle, Thierry Schaeverbeke, and Maria Kfoury. "Les limites des inhibiteurs de points de contrôle immunitaire et la gestion de leur toxicité." médecine/sciences 35, no. 12 (December 2019): 949–56. http://dx.doi.org/10.1051/medsci/2019191.
Baudoux, Nathalie, Grégoire Berthod, Frank Bally, Philippe Renard, and Sandro Anchisi. "Immunothérapie par inhibiteurs de points de contrôle immunitaire et hépatite." Revue Médicale Suisse 15, no. 651 (2019): 1017–21. http://dx.doi.org/10.53738/revmed.2019.15.651.1017.
Jaafar, Jaafar, Maria Mavromati, and Jacques Philippe. "Endocrinopathies induites par les inhibiteurs de points de contrôle immunitaire." Revue Médicale Suisse 14, no. 588-89 (2018): 34–38. http://dx.doi.org/10.53738/revmed.2018.14.588-89.0034.
Simand, Pierre-François, Grégoire Berthod, Laurent Parmentier, and Sandro Anchisi. "Immunothérapie par inhibiteurs de points de contrôle immunitaire et toxicité dermatologique." Revue Médicale Suisse 16, no. 695 (2020): 1086–91. http://dx.doi.org/10.53738/revmed.2020.16.695.1086.
Dieu-Nosjean, Marie-Caroline, and Christophe Caux. "La biologie des cibles PD-1 et CTLA-4 et la question des biomarqueurs." médecine/sciences 35, no. 12 (December 2019): 957–65. http://dx.doi.org/10.1051/medsci/2019192.
Delaunay, M., P. Caron, V. Sibaud, C. Godillot, S. Collot, J. Milia, G. Prévot, and J. Mazières. "Toxicité des inhibiteurs de points de contrôle immunitaires." Revue des Maladies Respiratoires 35, no. 10 (December 2018): 1028–38. http://dx.doi.org/10.1016/j.rmr.2017.08.006.
Wasielewski, E., and A. B. Cortot. "Critères d’évaluation de la réponse tumorale aux inhibiteurs des points de contrôle immunitaire." Revue des Maladies Respiratoires 35, no. 8 (October 2018): 828–45. http://dx.doi.org/10.1016/j.rmr.2017.06.007.
Дисертації з теми "Inhibiteurs de points de contrôle immunitaire":
Grasselly, Chloé. "Établissement et caractérisation de modèles précliniques de résistance aux inhibiteurs de points de contrôles immunitaires." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1256/document.
Because of the limited efficacy and the toxicity of conventional therapies to fight cancer, researchers focused on the new trategies. These efforts lead to the emergence of immunotherapies, whose msot recent actors are the monoclonal antibodies targeting immune checkpoint (ICP). Among those ICP inhibitors, we found antibodies targeting the surface protein « Programmed Cell Death 1 », called anti- PD1, and those targeting its ligand, « Programmed Cell Death Ligand 1 », called anti- PDL-1. Those antibodies shown a great efficacy in a wide diveristy of cancers, and are currently used for clinical practice in the case of melanoma, lung cancer, bladder cancer and renal cell carcinoma. However, those treatments don’t benefit to all tumor bearing patients, with a mean of 60% of innate resistance, and 25% of acquired resistance following a primary response, variable according to tumor type. Phenomena involved in resistance are currently poorly described. In this context, the aim of my project was to establish in vivo preclinical models of acquired resistance to anti-PD1 and anti-PDL-1. To do that, we used syngeneic renal cancer (RENCA), bladder cancer (MB49 and MBT-2), and colorectal cancer (MC38), and immunocompetent mice, that we have made resistant by serial reimplantations of tumors pieces and serial treatments, inducing a selection pressure until we obtained a resistant phenotype. The efficiency of PD1/PDL-1 axis blocking is strongly linked to the microenvironment composition, as a result we realized an immunophenotyping protocol. We observed anti-tumor cells as T cells, Natural Killer cells, and M1 macrophages, but also cells harboring immunosuppressive functions, as M2 macrophages, MDSC, and Treg. Moreover, some studies have identified an upregulation of alternatives ICP in the context of acquired resistance to anti-PD1, so we also observed the expression of LAG3, TIM3 and TIGIT besides PD1 and PDL-1 expression. We shown that resistance is strongly dependant to the tumor model, even if we identified a decrease of anti-tumor M1 macrophages is models resistant to anti-PD1, and an increase of Treg in models resistant to anti-PDL-1, suggesting a common mechanism of resistance specific to respectively anti PD1 and anti-PDL-1. Following Zaretsky and al. identification of genes involved in interferon pathway in the case of acquired resistance to anti-PD1 in melanoma, we decided to study the molecular profile of resistant tumors. We identified 5 common genes differently modulated between anti-PD1 and anti-PDL-1 resistant models, including SERPINF1 and FCNA which seems to be promising as targets to validate. Lastly, in parallel to establishment and characterization of preclinical models of acquired resistance, we tested new therapeutical approches of anti-PD1 and anti- PDL-1 potentiation in combination with reference chemotherapies. We shown a synergy in wild-type colorectal and bladder cancers (MC38 and MB49), no effect of the combination in metastatic breast cancer 4T1, and an inhibition of anti-PDL 1 effect in bladder cancer MBT-2. Immunphenotyping of tumors allowed us to observe here also high differences between tumor models, both at baseline and after treatments initiation. To conclude, even if our results need a validation with patients samples, we demonstrated that different cellular and molecular modifications could be involved in resistance to anti-PD1 and anti-PDL-1, and that resistance could be bypass with chemotherapy combination, according to tumor type
Tannous, Désirée. "The combination of Gadolinium-based nanoparticles, radiotherapy and immune checkpoint inhibitors : a novel therapeutic opportunity for cancer treatment." Thesis, université Paris-Saclay, 2022. http://www.theses.fr/2022UPASL082.
Scientific discoveries linked to radiotherapy are in continuous progress and almost 60% of cancer diagnosed patients are treated with radiotherapy. However, radiation therapy still faces many limitations due to radioresistance and the side effects inflected on healthy tissues. To overcome these factors, a particular interest has been aroused on the role that nanomedicine could play in the improvement of immune-mediated anti-tumor response. In this context, we decided to assess the ability of the combination of Gadolinium nanoparticles (AGuIX) with ionizing radiation (IR) to stimulate an anti-tumor immunological response and to increase the effectiveness of radiotherapy combined to immune checkpoint blockers.AGuIX are very small nanoparticles composed of a polysiloxane matrix and gadolinium chelates. Thanks to the magnetic properties of gadolinium, these nanoparticles play the role of a contrast agent, in addition to its radiosensitizing properties, thus allowing a better targeting and an enhanced therapeutic index.Our work reveals the ability of the AGuIX+IR combination to induce genomic instability and to stimulate immunomodulatory cell signaling pathways in treated human and murine cancer cells. In parallel, we demonstrate the anti-tumor activity of this combination by assessing tumor growth and overall survival using a preclinical model of immunocompetent mice bearing tumors. Our results strongly demonstrate a synergistic effect of AGuIX + IR combination on tumor growth and overall survival by stimulating the immune system. Finally, we reveal the capacity of AGuIX + IR combination to overcome immune checkpoint blockers resistance.In conclusion, our work shows that the combination of AGuIX+IR stimulates immunomodulatory signaling pathways, induces a strong synergistic anti-tumor response and helps overcoming resistance to immunotherapies
Liu, Peng. "Mort cellulaire immunogène induite par le crizotinib dans le cancer poumon non à petites cellules." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS148.
Accumulating evidence suggests that certain conventional chemotherapies, radiotherapies, as well as targeted therapies mediate their long-term therapeutic success by inducing immunogenic cell death (ICD), which stimulate the release or exposure of danger-associated molecular patterns from or on cancer cells, causing their recognition by the immune system, thus reinstating immunosurveillance. An unbiased screen identified crizotinib as a tyrosine kinase inhibitor that is potent in provoking hallmarks of ICD. In subsequent low-throughput validation experiments, crizotinib promoted Calreticulin exposure, ATP secretion, HMGB1 release, as well as ER stress in both human and murine cancer cells, especially if it is combined with normally non-ICD inducing chemotherapeutics such as cisplatin. ICD induced by the combination of chemotherapy and crizotinib was also observed in non-small cell lung carcinoma (NSCLC) cells lacking activating mutations of the crizotinib targets ALK and ROS1, suggesting an off-target-mediated mode of action. Comparative studies indicated that exclusively the clinically used (R) isoform of crizotinib was efficient in inducing cell death and stimulating ICD hallmarks whereas the (S) enantiomer lacked those characteristics. When combined with cisplatin, crizotinib-killed fibrosarcoma MCA205 cells as well as lung cancer TC-1 cells efficiently vaccinated syngeneic immunocompetent mice against a re-challenge with live cancer cells of the same types. Crizotinib improved the efficacy of chemotherapy with non-ICD inducers (such as cisplatin and mitomycin C) on three distinct (transplantable, carcinogen- or oncogene induced) orthotopic NSCLC models, none of which relied on the activation of ALK or ROS1. Of note these anticancer effects were completely lost if any of the ICD signals was blocked. These anticancer efficacies in different models were linked to an increased T lymphocyte infiltration as a sign of an immune response and were lost if such tumors grew on immunodeficient (nu/nu) mice that are athymic and hence lack thymus-dependent T lymphocytes, or on immunocompetent mice with a neutralization of interferon-. The combination of cisplatin and crizotinib led to an increase in the expression of CTLA-4, PD-1 and PD-L1 in tumors, coupled to a strong sensitization of NSCLC to immunotherapy with antibodies blocking CTLA-4 and PD-1. Hence, a combination of crizotinib, conventional chemotherapy and immune checkpoint blockade may be active against NSCLC, and these data might facilitate the design of clinical trials to evaluated novel combination regiments for the treatment of NSCLC
Hollande, Clémence. "Rôle de dipeptidyl peptidase-4 dans la régulation du trafic leucocytaire au cours du carcinome hépatocellulaire." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066446/document.
Dipeptidyl peptidase-4 (DPP4 or CD26)–mediated post-translational modification of chemokines has been shown to negatively regulate lymphocyte trafficking, and its inhibition enhances T cell migration and tumor immunity by preserving functional CXCL10. In extending these initial findings to humans and pre-clinical hepatocellular carcinoma models, we discovered a new mechanism whereby DPP4 inhibition improves anti-tumor responses by eosinophil recruitment. Specifically, administration of DPP4 inhibitors (DPP4i) resulted in higher concentrations of CCL11 (or eotaxin) and increased CCR3-mediated eosinophil migration into mouse tumors. Enhanced tumor control was observed upon treatment with DPP4i, an effect strikingly preserved in Rag2–/– mice, and abrogated only upon depletion of eosinophils or inhibition of their degranulation. We further demonstrated that tumor expression of IL-33 was necessary and sufficient for eosinophil-mediated anti-tumor responses, and that this mechanism contributed to checkpoint inhibitor efficacy. These findings provide new insight into IL-33- and eosinophil-mediated tumor control, revealed when endogenous mechanisms of DPP4 immune regulation are inhibited
Branchoux, Sébastien. "Critères de substitution de la survie globale chez les patients atteints de cancer métastatique traités par inhibiteurs de points de contrôle immunologiques." Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0253.
Advanced cancer treatment has been recently revolutionized by the development of the immune-checkpoint inhibitors (ICI). These immunomodulatory monoclonal antibodies are designed to either elicit a novel anti-tumoral immune response or revitalize an existing one to fight against cancer. Patients with cancer are living longer due to these improved therapies. Powering a study for overall survival (OS), the gold standard primary endpoint in randomized controlled trial (RCT) of anticancer drugs is becoming increasingly challenging. Therefore, it is of importance to identify and validate novel surrogate endpoints (SE) for OS in ICI-treated patients for expediting patients’ access to innovative and potentially life extending medicines. We first systematically reviewed published studies reporting on an association between alternative endpoints and OS in ICI-treated patients. Then, based on the learnings from this systematic literature review and from the specificity of the mechanism of action of ICIs, we evaluated the surrogacy properties of an emerging intermediate endpoint in solid tumors, namely time to next treatment (TNT), in ICI-treated patients with advanced melanoma and renal cell carcinoma (aRCC), through recent innovative statistical models for the validation of SE. Based on the results of these surrogacy analyses, TNT seems a promising SE for OS in RCTs of ICI-treated patients with advanced melanoma and aRCC. We encourage sponsors of RCTs of ICI to carefully collect the date of subsequent systemic treatment, so that surrogacy analyses could consequently be performed with a larger number of RCTs in order to confirm our findings
Cavelier, Cindy. "Etude du point de contrôle des dommages à l'ADN." Toulouse 3, 2010. http://thesesups.ups-tlse.fr/889/.
Acute Myeloid Leukemia (AML) is a clonal hematopoietic disorder characterized by the accumulation of malignant hematopoietic progenitor cells with an impaired myeloid differentiation program. The molecular basis of AML is thought to be associated with the acquisition of at least two types of critical cooperating mutations occurring at the hematopoietic stem or committed progenitors level. Class I mutations, affecting tyrosine kinases receptors and key components of cellular signalling pathways, confer growth and proliferative advantages. They are associated with class II mutations, affecting transcription factors thus leading to impaired normal differentiation program. In this study, we were first interested in CHK1, a protein kinase involved in preserving genome integrity by playing a critical role at the intra-S and G2/M cell cycle checkpoint activated in DNA damage response. We have shown that activation of CHK1 was sustained in immature cell lines, leading to a more stringent G2/M checkpoint in response to DNA damage, thus impairing illegitimate entry into mitosis in presence of unrepaired DNA damage and participating in their resistance to genotoxic agents. In a second study, we have demonstrated an abnormal activation of the CHK1 kinase in a large panel of AML patient samples, associated with the presence of constitutive DNA damage in absence of genotoxic stress. Moreover, the level of CHK1 activation is significantly correlated with unfavourable cytogenetic samples, particularly with complex karyotype phenotype. CHK1 inhibition by the pharmacological inhibitor UCN-01 or by RNA interference was found to decrease the clonogenic capacity of the AML progenitors, and to induce a chemosensitisation to ara-C. In contrast, growth of normal hematopoietic progenitors, which do not display constitutive DNA damage, was not impaired by such treatment. Overall, all these results underline the dual role of CHK1 kinase in AML pathology in the chemoresistance of immature leukemic cells and in the establishment of the genomic instability observed in complex karyotype AML. These findings could have major pharmacologic consequences, because they open a therapeutic window for new compounds targeting the cell cycle checkpoint machinery in AML and more particularly in the worst prognostic group with complex karyotype
Gagnon, Hugo. "Implications des proprotéines convertases lors d'infections : de l'activation du pathogène au contrôle de l’immunité." Thesis, Lille 1, 2012. http://www.theses.fr/2012LIL10179/document.
The proprotein convertases (PCs) are important enzymes mainly involved in the activation of protein precursors into the cell secretory pathway. This critical activation step that generates various biologically active polypeptides makes the PCs a cornerstone in a variety of biological process, including the neuroendocrine system. However, the PCs are described as very special players during infection, since they both activate various pathogens and control the immune response they induce. This thesis presents the development of a PCs peptide inhibitor for therapeutic purposes against pathogens and examines the role of PC1/3, which is mainly associated with the neuroendocrine system, in the control of the immune response in macrophages. As a first step, the PC inhibitor has been optimized by a peptidomimetic approach to block pathogens activation by PC for both a viral pathogen and a bacterial pathogen. In a second step, gene expression control tools have been used (shRNA) on a macrophage NR8383 cell line combined with the use of PC1/3 inactivated mouse (KO) to determine the physiological and molecular consequences of PC1/3 inactivation in macrophages by the mean of mass spectrometry approaches. The mass spectrometry approaches were proven to be a catalyst in this research and were further applied on ovarian cancer tissues studies, demonstrating the benefits of these tools. Overall, the results of this thesis demonstrate the feasibility of inhibiting PC to control infections and establish new avenues to modulate immunity by laying the foundations of PC1/3 molecular functions in the maintenance of immune homeostasis
Arakelian, Tsolère. "Impact of Targeting the Autophagy Related Gene Beclin 1 on the Immune Landscape of Melanoma." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS193.
Immune Checkpoint Blockades (ICBs)-based immunotherapy has emerged as a promising treatment for melanoma patients; however only a small subset of patients reaps a long term benefit. One of the major challenges to enhance the efficacy and extend the benefit of ICBs to non-responder patients is to design innovative approaches allowing the switch of “immune desert cold tumors” to “immune infiltrated hot tumors" which are eligible for ICB-based therapies. Here, we investigated the impact of targeting the early autophagy gene Beclin1 on the immune landscape of B16-F10 melanoma tumors. We found that targeting Beclin1 (Becn1-) significantly inhibited B16-F10 tumor growth and increased the infiltration of CD45+ leukocytes into the tumor bed. Immune phenotyping revealed an increased infiltration of active Natural Killer (NK) cells, inflammatory and resident type 1 macrophages, dendritic cells, and active CD8+ T lymphocytes. The inhibition of Becn1- tumor growth was no longer observed by depleting host CD8+ T cells, thus highlighting their major role in the control of Becn1- B16-F10 tumor development. We showed that Beclin1-dependent regulation of the immune landscape was associated with profound modulation of the cytokine/chemokine network in the tumor microenvironment (TME). Importantly, we revealed that Becn1- tumors displayed an inflammatory cytokine signature (comprised, but not restricted to, CCL5, CXCL10 and IFNg) that could be responsible for the switch from cold non T-inflamed to hot T-inflamed tumors. Mechanistically, we reported that the overexpression of IFNg in Becn1- TME was responsible for the induction of Programed Death ligand-1 (PD-L1) on tumor cells through the activation of JAK/STATs pathway. Overall, this study highlights Beclin1 as a valuable target, able to drive immune effectors cells into the melanoma tumors by inducing an inflammatory signature. This study provides the proof of concept for combining drugs inhibiting early autophagy process along with ICBs as a cutting-edge approach to improve their efficacy
Balança, Camille-Charlotte. "Contribution des réponses immunitaires adaptatives spécifiques des antigènes tumoraux à l'efficacité clinique de l'immunothérapie par inhibition de l'axe PD-1/PD-L1." Thesis, Toulouse 3, 2021. http://www.theses.fr/2021TOU30007.
Exhausted tumor-infiltrating lymphocytes (TILs) are characterized by immune checkpoint (IC) expression, for instance PD-1. One of the major immunotherapy approaches, based on IC inhibition, has proved efficient in the control of tumor progression in many cancers. Despite this progress, only a proportion of patients experience clinical benefit. To improve responses to IC inhibitors, understanding mechanisms involved in TIL exhaustion and investigating which T cells are able to respond to immunotherapy are required. We investigated both CD8 and CD4 T-cell exhaustion and its relation to tumor antigen (Ag) specificity and to responsiveness to IC inhibition in cancer patients. We demonstrated that CD8 T-cell exhaustion at the tumor site was only attained by tumor Ag-specific cells that were characterized by the sequential acquisition of ICs and by CD28 loss. Their circulating counterparts expressed less ICs and at lower levels and were CD28+. Specific CD8 TILs were dysfunctional, nonetheless, they maintained high cytotoxic potential and expressed tissue residency markers. We showed that PD-1 inhibition has a dual effect on specific CD8 T cells. It rescued their effector functions at the tumor site and enhanced their proliferation in the periphery. Importantly, the quantity of exhausted and specific TILs was predictive of response to therapy and of survival in patients treated with PD-1-targeting immunotherapy. Assessment of CD4 TIL exhaustion underscored similarities with the CD8 exhaustion program, in particular their specificity for tumor Ag and sequential acquisition of ICs although ICs characterizing terminally exhausted CD4 TILs were different than those found in CD8 TILs. Importantly, PD-1 blockade on CD4 TILs restored their helper functions, leading to dendritic cell maturation and, consequently, increased tumor-specific CD8 T-cell proliferation. Our data imply that under anti-PD-1/PD-L1, effector functions of terminally exhausted CD8 TILs is rescued and the tumor site is replenished by memory CD8 T cells which proliferate following direct blockade of PD-1 and through reinvigoration of the helper activity of tumor Ag-specific CD4 T cells. Our results position tumor Ag-specific T cells as major players of responsiveness to PD-1-blocking immunotherapy and identify predictive biomarkers of response to immunotherapy
Ben, Saad Elham. "Étude de l'endocytose du récepteur PD-1 dans les lymphocytes T humains." Thesis, 2019. http://hdl.handle.net/1866/23924.
PD-1 (Programmed Cell death protein -1) is a co-inhibitory receptor expressed on the surface of activated T cells. It plays an important role in maintaining peripheral tolerance and protecting against autoimmune and inflammatory diseases. However, permanent expression of PD-1 and its ligands PD-L1/ PD-L2 (PD-Ls) disrupts the immune response against pathogens and tumor cells. Immune checkpoint blockade (ICB) targeting the PD-1/PD-Ls axis has revolutionized the treatment of many cancers. Nivolumab (nivo) and pembrolizumab (pembro) are two anti-PD-1 monoclonal antibodies (mAb) that block the interaction between PD-1 and its ligands. They have shown promising results in the treatment of multiple types of cancers such as melanoma, non-small cell lung cancer, renal cell carcinoma, etc. Surprisingly, despite the success of anti-PD-1 in cancer immunotherapy, no-one has defined the destiny of surface PD-1 following antibody binding. Therefore, the objective of my master thesis was to define the fate of surface PD-1 following antibody binding and whether different anti-PD-1 Abs in the clinic differ in their ability to induce PD-1 endocytosis. The study of PD-1 endocytosis was performed on human T lymphocytes obtained from peripheral blood of healthy donors and activated with anti-CD3/anti-CD28 Ab or concanavalin A to express PD-1 receptor. Data analysis by flow cytometry showed that following anti-PD-1 Ab binding, 50% of PD-1 becomes endocytosed by 30min. In addition, we found that the PD-1 receptor is internalised upon its engagement with nivo and pembro and that most of the receptor is endocytosed within 30 min. However, 32 to 50% of the receptors are resistant to endocytosis. The comparative analysis of nivo and pembro has revealed a statistically significant difference (p=0.03) between the internalisation rate of the PD-1/nivo complex versus PD-1/pembro (46% versus 25% by 30min, respectively). Even at high concentrations of pembro, nivo induces better internalization of PD-1, suggesting that nivo could be more effective than pembro. Our study showed for the first time that ICB involves not only in the blockade of PD-1/PD-Ls interaction, but also in the endocytosis of PD-1 receptors from the surface of human T-cells, which differs between nivolumab and pembrolizumab. These results could be exploited to increase the therapeutic potential of nivolumab and pembrolizumab in cancer treatment. Keywords: PD-1 receptor, PD-1 ligands, T lymphocytes, Immune checkpoint blockade, Anti-PD1 antibodies, Nivolumab, Pembrolizumab, Endocytosis, Cancer
Частини книг з теми "Inhibiteurs de points de contrôle immunitaire":
Faury, Stéphane, and Jérôme Foucaud. "Immunothérapie spécifique, cancers et qualité de vie." In Pratiques et interventions en psychologie de la santé, 143–52. Editions des archives contemporaines, 2020. http://dx.doi.org/10.17184/eac.3192.