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Добірка наукової літератури з теми "Réponse à l'interféron"
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Статті в журналах з теми "Réponse à l'interféron"
Kaplanski, G., P. Cacoub, JM Durand, P. Bongranc, J. Soubeyrand, C. Farnarier, and JC Piette. "ICAM-1 soluble est un marqueur de réponse des hépatites C (VHC-HC) à l'interféron." La Revue de Médecine Interne 18 (May 1997): s85. http://dx.doi.org/10.1016/s0248-8663(97)80297-4.
Повний текст джерелаMaier. "Hepatitis – Hepatitisfolgen." Praxis 92, no. 33 (August 1, 2003): 1351–57. http://dx.doi.org/10.1024/0369-8394.92.33.1351.
Повний текст джерелаKhorsi, H., S. Castelain, J. Izopet, L. Stuyver, P. Zawadzki, D. Capron, F. Eb, and G. Duverlie. "Réponse au traitement par l'interféron alpha, et mutations dans la région NS5A, du virus de l'hépatite C." La Revue de Médecine Interne 17 (January 1995): S96. http://dx.doi.org/10.1016/0248-8663(96)86589-1.
Повний текст джерелаCacoub, P., P. Cresta, L. Frangeul, L. Musset, P. Opolon, J. M. Huraux, J. C. Piette, and F. Lunel. "Réponse à l'interféron alpha et disparition de la cryoglobulinémie chez les patients infectés par le virus de l'hépatite C." La Revue de Médecine Interne 17 (January 1996): 371s. http://dx.doi.org/10.1016/s0248-8663(97)80902-2.
Повний текст джерелаDi Martino, V. "Un nouveau facteur prédictif de réponse à l'interféron au cours de l'hépatite chronique C : la variabilité de la région NS5A." médecine/sciences 12, no. 12 (1996): 1448. http://dx.doi.org/10.4267/10608/696.
Повний текст джерелаJarrousse, B., S. Dautheville, F. Lhote, D. Méchali, P. Deny та L. Guillevin. "Vascularites systémiques viro-induites, co-infection virale B et C et réponse à l'interféron α: un virus peut-il en influencer un autre ?" La Revue de Médecine Interne 17 (січень 1995): S143. http://dx.doi.org/10.1016/0248-8663(96)86678-1.
Повний текст джерелаAlric, L., J. Izopet, ML Fort, P. Fontenelle, K. Sandre, S. Henri, M. Mularczyck та ін. "La réponse à l'interféron α au cours de l'hépatite virale C n'est pas modifiée par le système HLA de classe II: étude chez 120 patients". La Revue de Médecine Interne 18 (травень 1997): s85. http://dx.doi.org/10.1016/s0248-8663(97)80298-6.
Повний текст джерелаOuzan, D., N. Balarac, J. J. Renee, Ch Sattonet, J. M. Bidart, M. Greff, J. F. Rey, and M. F. Masseyeff. "Analyse multidimensionnelle des différents facteurs (âge, sexe, ferritinémie, bêta 2 microglobulinémie, transaminases et histologie) susceptibles d'influencer la réponse à l'interféron alpha des hépatites chroniques virales C." La Revue de Médecine Interne 13, no. 7 (December 1992): S349. http://dx.doi.org/10.1016/s0248-8663(05)80936-1.
Повний текст джерелаBOUDINOT, Pierre, and Abdenour BENMANSOUR. "Réponses antivirales des poissons : De l'interféron aux lymphocytes T." Bulletin de l'Académie vétérinaire de France, no. 2 (2007): 39. http://dx.doi.org/10.4267/2042/47865.
Повний текст джерелаДисертації з теми "Réponse à l'interféron"
Adalid-Peralta, Laura Virginia. "Rôle de l'interféron alpha dans la réponse anticorps au cours des pathologies infectieuses (VIH) et autoimmunes (Lupus)." Paris 11, 2006. http://www.theses.fr/2006PA11T068.
Повний текст джерелаLacroix-Lamandé, Sonia. "Rôle de l'interféron-γ dans la réponse immunitaire mucosale à l'infection par Cryptosporidium parvum chez la souris". Tours, 2001. http://www.theses.fr/2001TOUR4015.
Повний текст джерелаMaarifi, Ghizlane. "Rôle de SUMO (Small Ubiquitin-like Modifier protein) dans la réponse à l'interféron et la défense antivirale." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS135.
Повний текст джерелаSUMOylation modulates several cellular process including innate immunity and antiviral defense. Many key regulators involved in IFN induction, IFN signaling as well as various restriction factors are SUMOylated. Using cells stably expressing the different paralogs of SUMO; SUMO1, SUMO2 or SUMO3 and cells depleted of the only known SUMO conjugating enzyme, Ubc9, we show a differential effect on two viruses from Rhabdoviridae family (Vesicular Stomatitis Virus (VSV) and rabies virus) and on the response to IFN alpha and IFN gamma. First, we report that SUMO expression inhibits VSV- and rabies virus-induced IFN synthesis. Consequently, SUMO expression renders cells more sensitive to rabies virus infection. Overexpression of SUMO leads to IRF3 SUMOylation correlating rabies viral infection with both the inhibition of IRF3 activation and IFN beta synthesis. However, although SUMO inhibits VSV-induced IFN, SUMO confers resistance to VSV by inhibiting VSV primary transcription. Furthermore, the anti-VSV effect of SUMO is abolished in MxA depleted cells. Mechanistically, SUMO enhances MxA oligomerization resulting in the stabilization of the MxA protein. We also identified MxA as a new target of SUMO machinery. MxA interacts covalently with SUMO2/3 on lysine K48 and non-covalently with SUMO1. We then investigated the various roles of SUMO at different steps of the JAK/STAT pathway, including STAT activation, transcriptional response and IFN-induced biological effects, identifying SUMO as a new regulator of IFN response. The overexpression of SUMO leads to STAT1 SUMOylation and to a decrease in IFN-induced STAT1 phosphorylation resulting in an inhibition of IFN-gamma-induced transcription and biological responses. In contrast, SUMO expression does not alter IFN alpha signaling and transcriptional response. In addition, in SUMO3 expressing, IFN gamma;and IFN alpha induce SUMOylation of PML by SUMO3 inducing its degradation via the proteasome and inhibition of biological responses mediated by PML. Taken together our results show that SUMO plays a crucial role in innate and intrinsic immunity mediated by SUMOylated proteins such as IRF3, MxA, STAT1 or PML
Delbrel, Xavier. "Suivi après arrêt de l'interféron alpha des patients atteints de leucémie myéloi͏̈de chronique en rémission cytogénétique complète." Bordeaux 2, 1999. http://www.theses.fr/1999BOR23092.
Повний текст джерелаChaumont, Lise. "Functional study of key fish interferon-stimulated genes using an in vitro knock-out approach in fish cell lines : from comparative immunology to interest for vaccine production." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL038.
Повний текст джерелаIn jawed vertebrates, innate antiviral defenses are primarily based on type I interferons (IFNs). These master cytokines are secreted following virus recognition and induce the expression of hundreds of IFN-stimulated genes (ISGs). ISGs encode proteins with diverse functions, including enhancers of the type I IFN pathway and antiviral effectors, which all work towards establishing an antiviral state refractory to viral infection. Overall, the type I IFN system is well-conserved between mammals and fish but the ISGs repertoire is more diverse in fish, largely due to their complex evolutionary history and physiological specificities. Consequently, most mammalian ISGs have one or more orthologs in fish. However, it is still unclear whether fish ISGs are true functional homologs and their mechanisms of action remain to be explored in detail.In this context, my thesis aimed to functionally characterize two key fish ISGs, namely dsRNA-dependent protein kinase (pkr) and virus inhibitory protein endoplasmic reticulum-associated, interferon-inducible (viperin), by using an in vitro knock-out approach. In mammals, both proteins are primarily regarded as antiviral effectors: PKR is involved in host translation inhibition and apoptosis, while Viperin operates by generating antiviral ribonucleotides and modulating metabolic pathways exploited during viral life cycles. However, the extent to which these functions are conserved in fish remains largely unknown. The objectives of my thesis were articulated along three axes: (1) to develop and validate pkr-/- and viperin-/- fish cell lines using the CRISPR/Cas9 technology; (2) to functionally characterize these cell lines, in order to identify the mechanisms of action of fish PKR and Viperin and their role in regulating the type I IFN response through feedback loops; (3) to assess their permissivity to viral infections and their ability to produce viral particles at higher yields than their wild-type counterparts.Using complementary overexpression and knockout approaches, I first studied the molecular mechanisms of action of PKR in Chinook salmon (Oncorhynchus tshawytscha) CHSE-EC cells. Our findings show that salmonid PKR has conserved molecular functions, including apoptosis activation and inhibition of host protein synthesis. However, endogenous PKR did not play a major antiviral role during viral hemorrhagic septicemia virus (VHSV) infection. In fact, our results suggest that VHSV has evolved strategies to subvert PKR antiviral action, by limiting early induction of pkr expression, evading PKR-mediated translational arrest and taking advantage of PKR-mediated apoptosis at a late infection stage to favor viral spread.In parallel, we conducted a comparative RNA-seq analysis of the viperin-/- and wild-type fathead minnow (Pimephales promelas) EPC-EC cell lines with or without stimulation with recombinant type I IFN to have a global overview of the regulatory role of fish Viperin. Our data show that cyprinid Viperin is not involved in the regulation of the canonical type I IFN but negatively regulates specific inflammatory pathways. Our analysis further indicates that it plays a regulatory role in other metabolic processes, even in non-induced conditions, including extracellular matrix organization, cell adhesion and one carbon metabolism.During the development process of initial pkr-/- cell lines, two CHSE-EC cell lines were found to be persistently infected with infectious pancreatic necrosis virus (IPNV), presumably due to inadvertent contamination. I set out to characterize these persistently IPNV-infected cell lines over the course of 40 passages. A striking feature in both cell lines was the periodic oscillatory pattern of extracellular titers and intracellular viral RNA levels over passages. We further showed that the type I IFN response was not triggered during persistent infection, suggesting that persistent IPNV is able to evade the host innate immune response
Chabanon, Roman. "Exploiting DNA Repair Vulnerabilities to Modulate Anti-Cancer Immunity : a Study of the Immunological Potential of PARP inhibitors." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS007.
Повний текст джерелаPoly(ADP-ribose) polymerase inhibitors (PARPi) selectively target cancer cells with DNA repair deficiencies such as BRCA1/2 mutations or ERCC1 defects. Clinically, several PARPi are currently approved for the treatment of BRCA-mutant or platinum-sensitive advanced ovarian and breast cancers, and ongoing clinical trials are investigating the efficacy of PARPi in platinum-sensitive Non-Small Cell Lung Cancer (NSCLC). While PARPi constitute potent targeted therapies for the treatment of DNA repair-deficient malignancies, an increasing number of clinical trials are also evaluating their efficacy in combination with immune checkpoint inhibitor (ICI) in various populations. In this context, it is of critical importance to better understand how PARPi might modulate immune responses against cancer, and to investigate the inherent immunological potential of these agents.In this study, we show that ERCC1-defective NSCLC cells exhibit an enhanced type I interferon (IFN) transcriptomic signature and that low ERCC1 expression correlates with increased lymphocytic infiltration in human NSCLC tumours. Using isogenic cell lines and patient-derived xenografts, we further demonstrate that several clinical PARPi, including olaparib and rucaparib, display cell-autonomous immunomodulatory properties in ERCC1-defective NSCLC and BRCA1-mutant triple-negative breast cancer (TNBC) models. Mechanistically, PARPi generate cytoplasmic chromatin fragments with micronuclei characteristics; this activates the cGAS/STING pathway and elicits downstream type I IFN signalling and CCL5 secretion. Importantly, these effects are suppressed in BRCA1-reverted TNBC cells and ERCC1-rescued NSCLC cells, suggesting that DNA repair defects exacerbate the innate immunity-related phenotypes triggered by PARPi. Similarly, these effects are totally abrogated in PARP1-null TNBC cells, supporting the on-target effect of PARPi in mediating such phenotypes. Besides this potential to activate tumour cell-autonomous immunity through cGAS/STING and type I IFN signalling, we also observed that PARPi synergize with type II IFN to induce PD-L1 expression in NSCLC cell lines and fresh patient tumour cells, especially in the ERCC1-deficient setting. Moreover, we show that lethal concentrations of some PARPi independently activate the key damage-associated molecular patterns dictating the immunogenicity of cancer cell death, including calreticulin exposure at the tumour cell surface, ATP secretion and HMGB1 release in the extracellular compartment.Together, these preclinical data suggest that PARPi have intrinsic immunomodulatory properties that activate anti-cancer immune responses; this could be exploited clinically in combination with ICI in appropriately molecularly-selected populations
Martin, Élodie. "Étude de la modulation de la cascade de l'interféron suite à l'infection par le VIH." Thèse, 2005. http://hdl.handle.net/1866/15577.
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