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Academic literature on the topic 'Récepteur-1 de la chimiokine CX3C'
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Journal articles on the topic "Récepteur-1 de la chimiokine CX3C"
Chatel, M. A., A. Segret, T. Bourcier, C. Rucker-Martin, J. F. Renaud de la faverie, J. F. Charlin, V. Borderie, L. Laroche, and A. Lombet. "381 Intervention de la chimiokine SDF-1 et de son récepteur CXCR4 dans le contrôle de la néovascularisation cornéenne." Journal Français d'Ophtalmologie 28 (March 2005): 259. http://dx.doi.org/10.1016/s0181-5512(05)73502-6.
Full textDissertations / Theses on the topic "Récepteur-1 de la chimiokine CX3C"
Sirois-Gagnon, Dave. "Association entre l'obésité et des polymorphismes communs dans le récepteur de la fractalkine (CX3CR1)." Thèse, Université Laval, 2011. http://constellation.uqac.ca/217/1/030175066.pdf.
Full textChartral, Ugo. "Rôle de CX3CR1 dans l’immunité antitumorale médiée par les Lymphocytes T." Electronic Thesis or Diss., Bourgogne Franche-Comté, 2024. http://www.theses.fr/2024UBFCE007.
Full textThe MSS/MSI dichotomy in colorectal cancer (CRC) does not influence patient survival in the context of a strong immune infiltrate in terms of density and effector cells, also known as the "Immunoscore". However, the objective response rate to immunotherapies is much higher in MSI-CRC compared to MSS-CRC, despite the presence of an immune infiltrate within MSS CRC tumors. Since MSS metastatic colorectal cancers (MSS-mCRC) represent 95% of clinically observed cases, it is necessary to better understand the influence of the MSS-mCRC tumor microenvironment (TME) on CD8 T cells in order to develop new therapeutic strategies. Our research focused on CX3CR1, a G protein-coupled receptor (GPCR) whose role in antitumor immunity has been described as a biomarker for response to immunotherapies or chemotherapies and is also associated with cytotoxic functions in numerous infectious and tumor models. This thesis work aims to understand the role of CX3CR1 as a biomarker in cancers, investigate the mechanisms regulating its expression in the TME, and explore the role of CX3CR1 in antitumor immunity mediated by CD8 T cells infiltrating tumors and its potential use in optimizing cell therapies. We demonstrated that patients with mCRC who did not relapse after surgery had significantly higher expression of CX3CR1 on the surface of their CD8 T cells. While their tumor-infiltrating CD8 T cells did not express CX3CR1, we showed that the majority of these cells were CX3CR1+ CD8 T cells from the peripheral blood that had infiltrated the TME. TGF-β, secreted by the TME, induced a loss of CX3CR1 expression via miR-27a-5p in these cells. Moreover, our work demonstrated the role of the CX3CR1-CX3CL1 axis in potentiating the cytotoxic action of antigen-specific CD8+ T cells against cancer cells. Finally, the addition of this receptor in combination with a CAR-T cell construct potentiated the action of these cells. This work highlighted a potential tumor escape mechanism dependent on TGF-β, inhibiting the expression of CX3CR1 in tumor-infiltrating CD8 T cells and depriving them of the functional role of this receptor
Menasria, Rafik. "Implication des monocytes et des récepteurs CCR2 et CX3CR1 dans la réponse immunitaire innée suite à l'infection du système nerveux central par le virus herpès simplex 1 (VHS-1)." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27529.
Full textHerpes simplex virus 1 (HSV-1) is the main cause of sporadic viral encephalitis in developed countries with an annual incidence of 1/250 000 individuals per year. Despite the use of acyclovir that aimed at blocking virus replication, the mortality rate associated with HSV encephalitis (HSE) is still high (i.e., 30%), with the majority of surviving patients developing severe neurological sequelae. It is believed that the high mortality rate and neurological disorders attributable to HSE could involve both virally- and immune-induced damages of the central nervous system (CNS). The inflammatory response is initiated by the resident macrophages of the brain, namely microglia. In addition, blood leukocytes, particularly monocytes, are thought to infiltrate the CNS and contribute to the control of viral infection together with microglia. However, it is also argued that these cells may also amplify the inflammatory response, thereby contributing to brain damages. Knowledge concerning the recruitment of peripheral monocytes to the CNS and their role in the immune response during HSE is limited. A better understanding of the mechanisms involved in their dynamic of recruitment might lead to the identification of new therapeutic targets and the development of new strategies combining antiviral agents and immunomodulatory molecules to better control both HSV replication as well as the inflammatory environment in the CNS. The studies presented in this thesis are intended to better evaluate the involvement of monocytes-derived macrophages, together with microglia, in the cerebral innate immune response during experimental HSE. To achieve our goals, we first used chimeric mice in which bone marrow progenitor cells and blood leukocytes express the green fluorescent protein (GFP). This model allowed us to better characterize the kinetics of infiltration of blood monocytes into the CNS, their distribution in different anatomical areas of the brain and their involvement in the immune response during experimental HSE. The second part of the work focuses on the mechanisms involved in the recruitment of monocytes into the CNS and in the control of the inflammatory state in mouse brain following HSV-1 infection. More precisely, experiments aimed at characterizing the role of signaling pathways through chemokine receptors CCR2 and CX3CR1, expressed on the surface of blood monocytes and microglia, in protecting and modulating the recruitment of the two blood monocytes subtypes, namely the "inflammatory" and "patrolling" monocytes, during HSE. To achieve this aim, we used chimeric mouse models of CCR2- and CX3CR1-deficient animals, in which the lack of either receptor was restricted to the hematopoietic system (blood monocytes) or the CNS (microglia). Our results showed that blood monocytes are recruited to the CNS following HSV-1 infection and give rise to microglia-like macrophages. These cells are involved in the immune response together with microglia by performing immunological functions including phagocytosis and antigen presentation. Furthermore, we showed that CX3CR1 and CCR2 expressed on cells of the CNS and in the hematopoietic system, respectively, are important for mouse survival, viral replication control and in maintaining an appropriate inflammatory response during experimental HSE.
Désogère, Pauline. "Synthèse et étude de nouveaux agents chélatants optimisés ciblant le récepteur de chimiokine CXCR4." Phd thesis, Université de Bourgogne, 2012. http://tel.archives-ouvertes.fr/tel-00842206.
Full textRivière, Christel. "Fonction et régulation de l'activité de la chimiokine SDF-1 et de son récepteur CXCR4 dans la mégacaryopoïèse." Paris 11, 2000. http://www.theses.fr/2000PA11T054.
Full textMature megakaryocytes migration out of the bone marrow represents the ultimate step for platelet production and their release into the blood circulation. Regulation of this mechanism remains to be determined. Chemokines and their receptors play a major role in regulating cell migration towards specifie site, but also in cell retention. We studied the role of the SDF-I chemokine and its receptor CXCR4 during megakaryopoiesis. CXCR4 is expressed in megakaryocytes and platelets with an increasing expression during this differentiation process. Nevertheless, in opposite to CXCR4 expression, response to SDF-1 is down regulated during megakaryocyte maturation. CXCR4 signal transduction is mediated through heterotrimeric G protein αβγ. Using RT- PCR with degenerate oligonucleotides, we showed expression of severa! ROS proteins family members, negative regulators of G protein coupled receptor signaling, in megakaryocytes and platelets. RGS2 and RGS16 transcript levels, but not ROSI, RGS3 and ROSS, increase during megakaryocyte differentiation. Only these two ROS are transcriptionnaly upregulated in response to high concentrations ofSDF-1, revealing a specifie role in downregulating CXCR4 function. ROSI, RGS2, RGS3, and RGS16 overexpression in a megakaryocytic cellline MO7e and in megakaroyctes obtained in vitro lead to an inhibition ofSDF-1 response as weil as in migration and MAP kinases activation assays. This whole work implies CXCR4/SDF-I proteins in regulation of early stages of megakaryocyte migration. Our results suggest that upregulation of RGS2 and ROS16 expression during MK maturation plays a crucial role in CXCR4 loss of function and megakaryocyte release into the blood circulation
Sénécal, Vincent. "Expression et rôle de la fractalkine dans la neuro-inflammation associée à l'infection par le VIH-1." Doctoral thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/70266.
Full textBouamar, Hakim. "Etude de la régulation de la fonction du récepteur à chimiokine CXCR4 et rôle de CXCR7/SDF-1 dans l'hématopoïèse." Paris 7, 2010. http://www.theses.fr/2010PA077001.
Full textCouple CXCR4/SDF-1 plays a crucial role in the domiciliation of the HSC. The study of the regulation of the fonction of CXCR4 is crucial for better describing the mechanisms of migration, mobilization and retention of the hematopoietic original cells. One of the modes of regulation implies the accumulation of neutrophil elastase{NE) me cathepsinG (CG) associated with the cleavage of the N-terminal of CXCR4. We show that the murine form of CXCR4 is cleaved very quickly after treatment with NE and CG. The mutated forms of CXCR4 potentially resistant to the two enzymes which we generated are always sensitive to cleavage but the functional study of these mutants revealed that certain amino-acids are essential for CXCR4 signaling, The fonction of CXCR4 is also controlled by th0 extracellular concentration of SDF-1. We show that CXCR7 receptor is able to bind SDF- 1, is not expressed in thé hematopoietic cells whereas its expression is strong in stromal cell lines and primary stromal cells and that in overexpression, it confers neither the migratory capacity nor the activation of PI3K and MAPK pathways in response to SDF-1, However, CXCR7 can inhibit in a paracrine manner SDF-1 biological activities of cells expressing CXCR4, FinaHy, we showed that MS~5 stromal celis overexpressing CXCR7 inhibit the proliferation and hematopoiesis of human and murine hematopoietic immature cells by trapping SDF-1 of the extracellular medium strongly suggesting that CXCR7 is a "decoy receptor" which controls in a negative manner the fonction of CXCR4
Côté, Sandra. "Implication de la prostaglandine de Série E[indice inférieur 2] dans le contôle de l'expression du récepteur CCR7 chez les monocytes infectés par le virus de l'immunodéficience humaine de type I." Thèse, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/5115.
Full textOyegue, Liabagui Sandrine Lydie. "Contribution à l'analyse du déterminisme immunologique et génétique de la fibrose hépatique bilharzienne (schistosoma japonicum et mansoni)." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM5014.
Full textHuman infections with Schistosoma japonicum and Schistosoma mansoni causes hepatosplenic diseases leading to severe hepatic fibrosis in 5 to 30% of infected subjects living in endemic areas. Several studies demonstrated that the development of this fibrosis was regulated by cytokines but also by chemokines. Chemokines are the chemoattractant cytokines produced by a variety of immune and non-immune cells, and have been involved in the regulation of inflammation and granulomatous pulmonary and hepatic fibrosis in mice and humans. We therefore studied the modulation of chemokines and receptors in the liver and spleen of hepatosplenic patients exposed to infection with S.Japonicum. Our study demonstrates that the transcripts of CXC and CC chemokines and their receptors are increased in the liver of hepatosplenic patients, which were not significantly increased in the spleen during infection. This increase of transcripts of chemokines is not restricted to inflammatory chemokines, an increase of transcripts of homeostatic chemokines CCL19 and CCL21 is also observed in the liver of hepatosplenic patients. Moreover, the proportion of CD3+ lymphocytes but not CD14+ monocytes/macrophages is increased in the liver. We also observed a correlation of expression levels of CXCR3 ligands between them, in the liver of hepatosplenic subjects. These observations suggest that chemokines regulate hepatic inflammation induced by schistosoma eggs and probably play a role in liver fibrosis ensuing
Verrier, Thomas. "Function and plasticity of NKp46 expressing innate lymphoid cells." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC173/document.
Full textGroup 3 Innate Lymphoid cells (ILC3) actively maintain mucosal homeostasis through the production of Interleukin-22 (IL-22). ILC3 encompass 2 major populations, LTi (« Lymphoid Tissue inducer »), characterized by the expression of the chemokine receptor CCR6, and ILC3 that express the transcription factor T-bet, which include a population expressing the surface marker NKp46, a receptor originally used to identify group 1 ILC (ILC1). ILC1 plays a major role in the defense against intracellular pathogens and anti-tumoral responses. Three major ILC1 populations have been identified: the cytotoxic lymphocytes « Natural Killer » (NK or ILC1b), which largely rely for on the transcription factor Eomes their generation and express the integrin CD49b; hepatic and intestinal ILC1 that depends on the T-bet transcription factor and express CD49a (ILC1a); and a population that expresses CD49a and CD49b (ILC1ab) and populates the salivary gland and the uterus, which is independent of the transcription factor Nfil3. My work aimed to understand the biology of NKp46 expressing ILC, as well as factor involved in their development, maturation and function. The major part of my work focuses on NKp46+ ILC3. First, we demonstrate a major role for the chemokine receptor CXCR6 in their localisation in the lamina propria villi (Satoh-Takayama et al. 2014). Second, I showed that NKp46+ ILC3 could lose NKp46 expression (Verrier et al. 2016). Induced by TGFβ, this loss of expression was associated with higher IL-22 production and by the acquisition of markers identifying LTi (CCR6, MHC-II), demonstrating NKp46+ ILC3 plasticity. Finally, in collaboration with Rachel Golub’s group, we confirmed a putative role for Notch-signaling in this plasticity (Chea et al. 2016). In this manuscript, I will discuss the development and the heterogeneity of ILC3, ILC1a, ILC1b and ILC1ab. All the results I generated support a dynamic vision of ILC biology, which reflects how they adapt in response to environmental cues. By characterizing the different actors involved in this dynamic process, my work could be used to design therapies aiming at controlling the equilibrium between these different populations in diverse pathologies such as cancer, viral infection, or intestinal diseases