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Статті в журналах з теми "Activation de cellules immunitaires":
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.
Bensaïd, Albert, S. Bourdoulous, D. Lerhun, D. Calvez, L. Droogman, Dominique Martinez, and P. O. Couraud. "Expression d’interleukine 6 après infection par Cowdria ruminantium de cellules endothéliales de cerveau bovin." Revue d’élevage et de médecine vétérinaire des pays tropicaux 46, no. 1-2 (January 1, 1993): 195. http://dx.doi.org/10.19182/remvt.9360.
Vandestienne, Marie, Jérémie Joffre, Jérémie Lemarié, and Hafid Ait-Oufella. "Rôle du récepteur TREM-1 dans les maladies cardiovasculaires." médecine/sciences 38, no. 1 (January 2022): 32–37. http://dx.doi.org/10.1051/medsci/2021242.
Khamyath, Mélanie, Amélie Bonaud, Karl Balabanian, and Marion Espéli. "La signalisation de CXCR4, un rhéostat de la réponse immunitaire à médiation humorale." médecine/sciences 39, no. 1 (January 2023): 23–30. http://dx.doi.org/10.1051/medsci/2022192.
Cezard, Adeline, Sarah Monard, Déborah Bréa-Diakite, Antoine Guillon, and Mustapha Si-Tahar. "Les métabokines, des médiateurs essentiels de l’immunité anti-infectieuse." médecine/sciences 37, no. 4 (April 2021): 342–48. http://dx.doi.org/10.1051/medsci/2021031.
Hasan, Milena. "Milieu Intérieur." médecine/sciences 35, no. 5 (May 2019): 423–30. http://dx.doi.org/10.1051/medsci/2019077.
Deligne, Claire, and Laurent Gros. "Les anticorps monoclonaux anti-tumoraux." médecine/sciences 35, no. 12 (December 2019): 982–89. http://dx.doi.org/10.1051/medsci/2019194.
Salzet, Michel, and Robert Day. "Marqueurs endocriniens dans les cellules immunitaires : Notion de phénotype endocrinien." Journal de la Société de Biologie 197, no. 2 (2003): 97–101. http://dx.doi.org/10.1051/jbio/2003197020097.
Lebreton, Fanny, Charles-Henri Wassmer, Kevin Belofatto, Thierry Berney, and Ekaterine Berishvili. "Organoïdes sécréteurs d’insuline." médecine/sciences 36, no. 10 (October 2020): 879–85. http://dx.doi.org/10.1051/medsci/2020129.
Milliat, Fabien, and Agnès François. "Les mastocytes, stakhanovistes de l’immunité." médecine/sciences 34, no. 2 (February 2018): 145–54. http://dx.doi.org/10.1051/medsci/20183402012.
Дисертації з теми "Activation de cellules immunitaires":
Ouedraogo, Richard. "La spectrométrie de masse : application à l'étude des cellules immunitaires." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5062/document.
In view of the many advantages in terms of speed, cost , sensitivity and reliability of the MALDI -TOF mass, we thought we could apply it to the study of intact eukaryotic cells, in particular the study of cells immune . We have shown that this approach is applicable to the global analysis of eukaryotic cells including circulating immune cells. In addition, it allowed us to characterize the many faceted of human macrophage activation by analyzing the data with the R software library " MALDIquant " and specific algorithms. The protein/peptide fingerprint induced by the M1 agonists : IFN - γ , TNF , LPS and LPS + IFN - γ or M2 agonists : IL- 4 , TGF - β1 and IL- 10 are distinct to unstimulated macrophages and specific for each agonist. MALDI -TOF Mass spectrometry can then be used to characterize the subtypes M1 and M2 macrophages . In addition, fingerprints induced by extracellular bacteria ( group B streptococcus , Staphylococcus aureus ) are specific and closed to those induced by IL -4 . The responses of macrophages to intracellular bacteria (BCG, Orientia tsutsugamushi , Coxiella burnetii ) are also unique. Mass spectrometry MALDI -TOF of whole cell revealed therefore the multifaceted activation in human macrophages . Finally, preliminary results show that our approach could be used clinically for the analysis of circulating cells in the case of host-pathogen interaction
Al, Hajj Sally. "Effets des concentrations élevées en chlorure de sodium sur les fonctions immunitaires des cellules dendritiques." Electronic Thesis or Diss., Tours, 2019. http://www.theses.fr/2019TOUR3309.
Recent evidence showed that in response to elevated sodium dietary intakes, many body tissues retain Na+ ions for long periods to reach concentrations up to 200 mM. Recent studies suggested that the immune system might be the bridge linking high sodium intake to several cardiovascular diseases and cancer progression as well. However, the studies about the effects of sodium on immunity brought about contrasted results. So far the effects of sodium on human dendritic cells (DCs) remain unknown. Considering their central role in the immune response, we tested how sodium chloride-enriched medium influences the immune properties of human DCs. DCs were derived from CD14+ monocytes from healthy donors and then stimulated by LPS, in sodium-enriched medium (from 140 up to 200 mM) and finally analyzed. We found that DCs cultivated in high Na+ concentrations remain viable and maintain the expression of DC markers up to 200 mM. In response to LPS, their maturation, their chemotaxis toward CCL19, their production of pro-inflammatory cytokines and ROS were inhibited by high [Na+]. In line with these results, we report that the T-cell allostimulatory capacity of DCs was also inhibited. Finally our data indicate that these effects were mediated through the phosphorylation of SGK-1 (serum and glucocorticoid induced kinase-1) and ERK1/2 kinases.Our results raised the possibility that the effects of sodium on T-cells might be counterbalanced by its ability to downregulate DC activation. Therefore the effects of high sodium diet on the immune response might be more complex than previously thought
Boitelle, Agnès. "Mécanismes de recrutement et de régulation de l'activité des macrophages alvéolaires, dans un contexte de pathologie interstitielle pulmonaire." Lille 1, 1997. https://pepite-depot.univ-lille.fr/LIBRE/Th_Num/1997/50376-1997-85.pdf.
LOOR, PATRICE. "Signalisation via tyrosine-kinases dans l'activation des cellules t : etude par technique biosensor des interactions entre grb2 et dynamine." Strasbourg 1, 1995. http://www.theses.fr/1995STR15018.
Bercovici, Nadège. "Activation et induction de tolérance des lymphocytes T dans des modèles de souris transgéniques." Paris 11, 1999. http://www.theses.fr/1999PA11T030.
Antigen recognition by T cell can lead to immunity but also to antigen-specific T-cell tolerance. Immunological tolerance can be induced experimentally and may be useful for the treatment of organ-specific autoimmune diseases such as autoimmune diabetes. In this work, I have investigated the mechanisms of activation and tolerance induction in mature CD4+ and CDS+ T cells from TCR-transgenic mice. Systemic administration of soluble peptide is remarkably efficient to induce peripheral T-cell tolerance in vivo. Although one single injection induced transient T-cell tolerance, chronic intravenous (i. V. ) injections of soluble peptide is able to maintain CD4+ T-cell tolerance for more than 12 weeks. I have also shown that i. V. Injection of soluble peptide can tolerize naive CDS+ T cells but can also target effector CDS+ T cells thereby blocking the progression of an ongoing CDS-mediated autoimmune diabetes. Importantly, CDS+ T cell infiltrates are eliminated without bystander tissue damage. Furthermore, I have demonstrated that i. V. Injection of soluble MHC class I : peptide complexes represent an alternative strategy to induce CDS+ T cell tolerance in vivo. Tolerance was achieved by deletion and anergy of antigen-specific CDS+ T cells and allow to down-regulate an ongoing CDS mediated autoimmune diabetes. In experiments conducted in vitro with naïve T cells from TCR-transgenic mice, we have shown that antigen recognition by CD4+ T cells rapidly induced cytoskeletal alterations that are crucial for calcium responses and proliferation. Under conditions in which equal numbers of specific MHC class Il :peptide complexes are presented by dendritic cells (DC) and B cells, we could demonstrate that DC are always more efficient antigen presenting cells underlying the importance of adhesion/costimulatory molecules abundantly expressed by DC. Moreover, we provide evidence for the induction of small calcium signals in CD4+ T cells interacting with DC in the absence of specific antigen that involve MHC/TCR interactions. Finally, we have shown that naive CDS+ T cells can be fully activated and differentiated after antigenic stimulation in the absence of co-stimulatory signals. Altogether, these data contribute to our understanding of the mechanisms of activation and tolerance induction of CD4+ and CDS+ T cells
Miloro, Giorgia. "Déterminer le rôle du récepteur de mort Fas/CD95 dans la co-stimulation des cellules T." Electronic Thesis or Diss., Université Côte d'Azur, 2020. http://www.theses.fr/2020COAZ6036.
Fas (CD95/TNFRSF6), a type-I transmembrane receptor of the tumor necrosis factor receptor (TNFR) superfamily, is a well-known cell death activator. However, it has been also implicated in non-cell death processes including cell survival, differentiation, migration. Whereas the molecular cascade that initiates apoptosis upon Fas engagement with its ligand FasL is particularly well described, the informations concerning the molecular mechanisms underlying the Fas mediated non-apoptotic pathways are sparse.As indicated by the induction of autoimmunity and lymphoproliferation in ALPS patients harboringmutations in either the receptor or its ligand, the Fas/FasL system plays a major role in T cell immune homeostasis and thus, in the control of autoimmunity and cancer. On one side, the Fas mediated death has been described critical for (i) the deletion of autoreactive lymphocytes, and thus in the maintenance of peripheral tolerance; (ii) the control of the number of lymphocytes activated by weak antigens during pathogen infections.On the other side, and beyond cell death induction, some Fas non-death pathways have been described in T cells, among which the role of Fas as co-regulatory receptor for the TCR during its activation. Despite the potential importance of this role in immunotherapeutic strategies, only few and controversial studies related to this involvement were done. Indeed, whereas several studies have described Fas as a TCR co-stimulatory receptor, others defined an inhibition of T cell activation by Fas-TCR concomitant stimulation. In this context, the aim of my PhD project consisted into molecularly dissect the Fas-TCR co-signaling.By using both primary T cells and cell lines bearing a specific transgenic TCR, we could define Fas as a costimulatory receptor. By exploiting biochemical approaches as well as flow cytometry and microscopy we could decipher the Fas-TCR crosstalk both at functional and molecular level. First, we show that Fas-TCR costimulation occurs in both naïve and in memory T cells as well as in both CD4+ and CD8+ T cell subpopulations.Molecularly, we could describe that Fas enhances the TCR signaling at membrane proximal level, since the phosphorylation of the first proteins involved in TCR activation is increased. Furthermore, both membrane-bound and soluble FasL are capable to initiate Fas co-stimulatory signal. Lastly, we could exclude the involvement of FADD and Caspase-8, first actors of Fas signaling, in the co-activation, and even more importantly, the involvement of the death domain of Fas cytoplasmic tail, unveiling the implication of another Fas receptor domain. To describe the molecular mechanisms and the context where Fas-TCR co-stimulation occurs might be of an outstanding importance in the comprehension of Fas physiopathology in T cells and for future studies that might involve its potential for immunotherapeutic strategies
Chevalier, Mathieu. "Sous-populations lymphocytaires T régulatrices et réponses Th17 en primo-infection VIH : rôle dans le contrôle de l'activation immunitaire." Paris 7, 2013. http://www.theses.fr/2013PA077017.
Generalized and persistent immune activation plays a central role in the pathogenesis of HIV infection. The immune activation set point, as defined by CD8 T-cell activation at the end of primary HIV infection (PHI), is predictive of disease progression (CD4 T-cell loss). The aim of this study was to identify early mechanisms that could be involved in the control of systemic immune activation. Twenty-seven patients with PHI were enrolled in a prospective longitudinal study with a 6 month follow-up. We showed that there was no evidence for a role of natural regulatory T cells in the control of immune activation during PHI. However, our data suggest that double-negative T cells could be able to dampen immune activation, probably via the production of anti-inflammatory cytokines. Microbial translocation is thought to be one of the major causes of immune activation in the chronic phase of HIV infection. In our study, the Th17/Treg ratio was negatively correlated to the level of T-cell activation and to monocyte activation (measured by the plasma levels of soluble CD14 and IL-1RA). However, we demonstrated that systemic microbial translocation did not occur during the phase of PHI in the great majority of patients. Thus, data indicate that T-cell and monocyte activation observed in PHI mostly result from viral replication and not from microbial translocation. Interestingly, plasma levels of soluble CD14 and IL-1RA at baseline were predictive of the T-cell activation set point. These plasma soluble proteins may be considered for use in clinical practice as early surrogate markers for disease progression
Achard, Carole. "Le virus oncolytique de la rougeole : sensibilité du mésothéliome pleural malin et activation du système immunitaire." Nantes, 2016. https://archive.bu.univ-nantes.fr/pollux/show/show?id=f2d251a0-7c4c-48bf-bcfb-f3839dd6159c.
I worked on an antitumor virotherapy strategy based on the use of an attenuated strain of measles virus (MV) to treat malignant pleural mesothelioma (MPM). It is described that MV preferentially infects tumor cells which overexpress its major receptor CD46 on their surface. By studying in vitro 22 human MPM cell lines, I demonstrated that 70% of the MPM cell lines are sensitive to the infection and that the sensitivity to MV depends on defects of their antiviral type I interferon (IFN) response rather than on the overexpression of CD46. Healthy cells are not sensitive to MV since they develop a full type I IFN response. Thus, 70% of patients may be sensitive to this therapeutic approach. It is admitted that MV induces immunogenic death of tumor cells, which is able to activate dendritic cells (DCs) and their capacity to cross-present tumor antigens. I continued to characterize the effects of MV on DCs and I showed that blood myeloid CD1c+ DCs and plasmacytoid DCs (pDCs) express TRAIL on their surface in response to MV. This TRAIL expression depends on their IFN-α secretion which is induced by the detection of viral RNA by the cytosolic sensors RLRs (RIG-I like receptors) in both types of DCs, and by TLR7 (Toll-like receptor 7) activation in pDCs only. These DCs are then able to induce the lysis of TRAILsensitive cells. Altogether, my results lead to a better understanding of the oncolytic activity of MV, which relies not only on the infection and lysis of tumor cells but also on the activation of the immune system against tumors
Yatim, Nader. "Coordinated activation of cell death and inflammatory pathways in dying cells regulate adaptive immunity." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC233.
Dying cells initiate adaptive immunity by providing both antigens and inflammatory stimuli for dendritic cells (DCs), which in turn activate CD8' T cells through a process called antigen cross-priming. To define how different forms of programmed cell death influence immunity, we established models of necroptosis and apoptosis, where dying cells are generated by RIPK3 and CASP8 dimerization, respectively. We found that release of inflammatory mediators such as damage-associated molecular patterns (DAMPs) by dying cells was not sufficient for CD8+ T cell cross-priming. Instead, robust cross-priming required RIPK1 signaling and NF-KB-induced transcription within dying cells. Decoupling NF-1(13 signaling from necroptosis or inflammatory apoptosis reduced priming efficiency and tumor immunity. Our results reveal that coordinated inflammatory and cell death signaling pathways within dying cells orchestrate adaptive immunity
Herblot, Sabine. "Etude des mécanismes moléculaires impliqués dans la différenciation et l'activation des cellules du système immunitaire : différenciation des macrophages, activation des lymphocytes T par l'IL-2." Bordeaux 2, 1997. http://www.theses.fr/1997BOR28518.
Книги з теми "Activation de cellules immunitaires":
International Conference on Lymphocyte Activation and Immune Regulation (9th 2002 Newport Beach, Calif.). Lymphocyte activation and immune regulation IX: Homeostasis and lymphocyte traffic. New York: Kluwer Academic/Plenum Publishers, 2002.
Fondation IPSEN pour la recherche thérapeutique. Meeting. The role of platelet-activating factor in immune disorders: Proceedings of the Meeting of the "Fondation IPSEN pour la recherche thérapeutique", Paris, June 25-26, 1987 (part II). Edited by Braquet P. Basel: Karger, 1988.
Sudhir, Gupta, and International Conference on Mechanisms of Lymphocyte Activation and Immune Regulation (5th : 1994 : Newport Beach, Calif.), eds. Mechanisms of lymphocyte activation and immune regulation V: Molecular basis of signal transduction. New York: Plenum Press, 1994.
J, Mond James, Cambier John C. 1948-, and Weiss Arthur 1952-, eds. Cell activation: Genetic approaches. New York: Raven Press, 1991.
Varmus, Harold. Genes and the biology of cancer. New York: Scientific American Library, 1993.
Libero, Gennaro De. T cell protocols. 2nd ed. New York: Humana Press, 2009.
N, Serhan Charles, and Ward Peter A. 1934-, eds. Molecular and cellular basis of inflammation. Totowa, N.J: Humana Press, 1999.
(Editor), Sudhir Gupta, Eugene Butcher (Editor), and William E. Paul (Editor), eds. Lymphocyte Activation and Immune Regulation IX: Homeostasis and Lymphocyte Traffic (Advances in Experimental Medicine and Biology). Springer, 2007.
Becker, Elmer L. Membrane Activation in Immunologically Relevant Cells (Chemical Immunology). S. Karger AG (Switzerland), 1988.
(Editor), Marc Daeron, and Eric Vivier (Editor), eds. Immunoreceptor Tyrosine-based Inhibition Motifs (Current Topics in Microbiology and Immunology). Springer, 1999.