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Статті в журналах з теми "Homéostasie – génétique"
Hasan, Milena. "Milieu Intérieur." médecine/sciences 35, no. 5 (May 2019): 423–30. http://dx.doi.org/10.1051/medsci/2019077.
Повний текст джерелаДисертації з теми "Homéostasie – génétique"
Ruchat, Stéphanie-May. "Étude des déterminants génétiques et des interactions gène-gène et gène-environnement associés à l'homéostasie glucidique." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26878/26878.pdf.
Повний текст джерелаWang, Ying. "Genetic dissection of adaptor molecules in lymphocyte development, homeostasis and function." Aix-Marseille 2, 2006. http://www.theses.fr/2006AIX22035.
Повний текст джерелаL’adaptateur transmembranaire LAT (Linker for Activation of T cells) constitue une plateforme moléculaire assurant le recrutement de nombreuses protéines impliquées dans la transduction des signaux médiés par le TCR. Les souris homozygotes pour une mutation ponctuelle de la tyrosine 136 du domaine intracytoplasmique de LAT présentent un défaut dans le développement des lymphocytes T. En outre, elles développent progressivement une lymphoprolifération T CD4+ polyclonale qui est associée à une éosinophilie tissulaire et à une maturation massive des cellules B en plasmocytes sécrétant des niveaux élevés d’IgG1 et d’IgE. Pour disséquer les mécanismes cellulaires et moléculaires associés au développement de cette pathologie, nous avons mis en oeuvre un système de transfert adoptif à court terme et à long terme dans des hôtes présentant une immunodéficience sélective en lymphocytes T. Nous avons montré que les cellules T CD4+ des souris mutantes LATY136F présentent une homéostasie similaire à celle des cellules wt en début de reconstitution. En revanche, 8 semaines après reconstitution, les cellules T CD4+ desLATY136F induisent une pathologie lymphoproliférative qui reproduit en tout point celle observée initialement dans les souris LATY136F. Ainsi, les souris reconstituées présentent-elles une accumulation massive de cellules T CD4+ et de lymphocytes B dans les organes lymphoïdes secondaires, une ypergammaglobulinémie IgG1 et IgE et une éosinophilie marquée dans de nombreux tissus. Ceci démontre que les lymphocytes T sont nécessaires et suffisants pour induire la pathologie LATY136F. Par comparaison des reconstitutions réalisées dans des hôtes déficients en CD3 et exprimant ou non les molécules d’histocompatibilité de classe II, nous avons établi que les lymphocytes T CD4+ LATY136F conservent, en l’absence de molécules d’histocompatibilité de classe II, leur capacité à proliférer et à stimuler la maturation des lymphocytes B en plasmocytes sécrétant des IgG1 et des IgE -avec une efficacité néanmoins deux fois moindre-. Ces résultats suggèrent que la lymphoprolifération des cellules T CD4+ dans les souris mutantes LATY136F et que la coopération T/B associée qui conduit à des concentrations sériques considérables d’IgE et IgG1 sont, pour une large part, indépendants des moléculesd’histocompatibilité de classe II. Ce comportement largement indépendant du TCR et pouvant à ce titre être qualifié de comportement autistique vis-à-vis des molécules de classe II apparaît comme une propriété unique des cellules T CD4+ portant la mutation LATY136F. NTAL (Non T cell Activation Linker, également appelé LAB) est un adaptateur transmembranaire récemment identifié qui possède des similarités structurales avec LAT. NTAL est fortement exprimé dans les cellules B, les cellules NK et les mastocytes. NTAL est rapidement phosphorylé par les kinases de la famille Src (Lck ou Fyn) et de la famille Syk (Zap-70 ou Syk) après engagement du récepteur des cellules B (BCR) ou des récepteurs au fragment Fc des immunoglobulines de type FcγRI et FcεRI. Les principales protéines identifiées comme associées à la molécule NTAL phosphorylée sont Grb2, SOS1, C-Cbl, Gab1. La suppression de l’expression de NTAL dans une lignée B conduit à une diminution des flux calciques et de l’activation des molécules Erk, ce qui suggère que NTAL participe à l’induction des flux calciques et à l’activation de la voie Ras-MAPKassociées à la stimulation du BCR. Pour identifier les rôles respectifs de NTAL et de LAT dans le développement et la fonction des lymphocytes B, des souris déficientes pour Ntal ont été générées et croisées avec des souris déficientes pour LAT. L’ analyse de ces souris a montré que les cellules B se développent avec la même efficacité dans les souris doublement déficientes Lat-/-Ntal-/-, dans les souris déficientes dans l’un de ces deux gènes et dans les souris wild-type, ce qui démontre que NTAL n’est pas indispensable pour le développement des lymphocytes B. L’agrégation des récepteurs des cellules B induit, par ailleurs, des niveaux de prolifération et des niveaux de flux calciques légèrement augmentés dans les souris déficientes pour Ntal. L’analyse des réponses humorales T dépendantes et T indépendantes a montré que les souris déficientes pour Ntal possèdent, en outre, des niveaux augmentés d’anticorps naturels et des réponses humorales légèrement amplifiées en réponse à des antigènes T dépendants. Des titres normaux d’immunoglobulines sériques spécifiques sont observés en réponse à des antigènes T indépendants. Enfin, bien que NTAL soit également exprimé dans les plasmocytes, son absence n’affecte pas l’hypergammaglobulinémie E et G1 sedéveloppant dans les souris porteuses de la mutation LATY136F. NTAL ne constitue donc pas dans les lymphocytes B l’équivalent fonctionnel de LAT dans les lymphocytes T
Mingueneau, Michaël. "Dissection génétique du récepteur pour l'antigène des lymphocytes T : codage proximal et conversion du signal "ligand", de sa reconnaissance à l'assemblage des signalisomes." Aix-Marseille 2, 2008. http://theses.univ-amu.fr.lama.univ-amu.fr/2008AIX22067.pdf.
Повний текст джерелаThe mechanisms by which ligand recognition is encoded and converted into a cytoplasmic signal by the T cell receptor (TCR), in particular how signals are initiated and terminated and how this code is adjusted during T cell differenciation are central themes in T cell immunology and constitute the subject of this work. Two main models have been proposed to account for signal initiation following ligand recognition by the TCR. In one model of T cell activation, the half‐lives of TCR:pMHC complexes constitute the main parameter driving T cell activation. In an alternative model, conformational changes of the receptor have been proposed to rationalize the seminal events leading to biochemical cascades. In particular, in one of the most recently advocated conformational model of T cell activation, a proline‐rich motif (PRS) located in the cytoplasmic tail of CD3ε has been proposed to be inducibly exposed following activation and to recruit the cytosolic adaptor NCK. According to that model, this step would occur even prior to phosphorylation events and would constitute a critical step for T cell activation. To assess this model, we constructed a knock‐in mouse deprived of this sequence. The phenotype of this mouse invalidated the conformational model of T cell activation based on an inducible exposure of this motif. Unexpectedly this mouse also unraveled novel functions for the PRS sequence at the β selection checkpoint, but also during γδ selection events and turned out to be a crucial regulator of TCR levels expressed on DP thymocytes and also required for positive selection events. These four functions were linked to the constitutive interaction between CD3εPRS and NCK and to the recruitment of LCK by NCK. Although this last interaction has to be directly demonstrated, the compensation of the phenotype by a pre‐activated LCK kinase strongly suggests that the functions associated with CD3εPRS:NCK interaction are mediated through LCK. These observations led us to formulate a model in which a tri‐molecular complex composed of CD3εPRS:NCK:LCK constitutes an intracellular coreceptor recruiting LCK in situations where the TCR is not or not efficiently coupled with CD4 and CD8 coreceptors, i. E. During β selection, γδ selection, in pre‐selected CD4+CD8+ thymocytes and during positive selection (where thymocytes recognize low‐affinity ligands that do not recruit efficiently the coreceptors due to the short half‐life of these ligands). Lastly, the function associated with the CD3εPRS in CD4+CD8+ thymocytes was linked to the participation of this sequence to a degradation pathway mediated by SLAP and c‐CBL leading to CD3ζ ubiquitination and degradation. In order to analyze signals that participate to the termination of activatory signals, we used the LatY136F/Y136F mouse genetic model in which the LAT adaptor is deprived of the tyrosine 136 and which develops a CD4 lymphoproliferative disorder. To understand the mechanisms at play in this pathology, we developed a conditional model allowing the expression of the mutation in peripheral T cells. This approach demonstrated that this disorder is not mediated by an auto‐immune mechanism and that a similar pathology occurs in complete absence of LAT adaptor, suggesting that altered LAT signals do not participate to the unfolding of the disease. Interestingly, the absence of LAT molecules led to the exacerbation of some of the biochemical events, unraveling in a direct fashion the negative regulatory function of LAT for T cell homeostasis
Pang, Yuanyu. "Caractérisation des cellules régulatrices CD4+CD25+FOXP3+ dans des conditions homéostatiques et au cours du GVHD." Paris 7, 2014. http://www.theses.fr/2014PA077013.
Повний текст джерелаUnderstanding the heterogeneity of human CD4+FOXP3+ regulatory T cells (Treg) and their potential for lineage-reprogramming is of critical importance for moving Treg therapy into the clinics. Using multi-parameter single-cell analysis techniques we explored the heterogeneity and functional diversity of human Treg in healthy donors and in patients after allogeneic hematopoietic stem cell transplantation (alloHSCT). Human Treg displayed a level of complexity similar to conventional CD4+ effector T cells with respect to the expression of transcription factors, homing receptors and inflammatory cytokines. Single-cell profiling of the rare Treg producing IL-17A or IFN-y showed an overlap of gene expression signatures of Th17 or TH1 cells and of Treg. To assess if Treg homeostasis is affected by an inflammatory and lymphopenic environment, we characterized the Treg compartment in patients early after alloHSCT. This analysis suggested a marked depletion of Treg with a naive phenotype in patients developing acute graft-versus-host disease, compared to tolerant patients. However, single-cell profiling showed that CD4+FOXP3+ T cells maintain the Treg gene expression signature and Treg suppressive activity was preserved. Our study establishes that heterogeneity at the single-cell level, rather than lineage-reprogramming of CD4+FOXP3+ T cells, explains the remarkable complexity and functional diversity of human Treg
Thomas, Charles. "Impact du cholestérol sur le cycle entérohépatique des acides biliaires : conséquences pour l'homéostasie lipidique." Dijon, 2006. http://www.theses.fr/2006DIJOS016.
Повний текст джерелаHypercholesterolemia is a major risk factor of cardiovascular diseases. Understanding of mechanisms ensuring the maintenance of body cholesterol homeostasis is crucial, since it can allow the development of new hypocholesterolemiant therapies. Bile Acids (BA) are end-products of cholesterol metabolism. These molecules, produced in the liver, participate to fat digestion and absorption in the intestine. Moreover, BA represent the main pathway of body cholesterol removal. The results presented in this thesis show that genes encoding intestinal, hepatic and renal BA transporters are coordinately regulated. This mechanism ensures efficient BA elimination through faecal and urinary route, and thus contributes to explain the resistance of mice to diet-induced hypercholesterolemia. The transcription factors SREBP-2 and HNF-1, and the nuclear receptor PPAR, play a key role in this adaptative process since they allow cholesterol-dependent regulation of several key BA transporters, particularly ASBT in the ileum and the kidney, and L-FABP in the liver
Demény, Maté Agoston. "Analysis of TAF8, a subunit of TFIID and SMAT (smal TAF complex), reveals novel regulation of the assembly of TAF-containing complexes." Université Louis Pasteur (Strasbourg) (1971-2008), 2006. http://www.theses.fr/2006STR13096.
Повний текст джерелаRoy, Gauthier. "Étude d'un système d'acquisition du cuivre chez Bordetella pertussis : nouveau mécanisme de régulation post-transcriptionnelle et caractérisation fonctionnelle préliminaire." Electronic Thesis or Diss., Université de Lille (2022-....), 2022. http://www.theses.fr/2022ULILS058.
Повний текст джерелаSeveral transition metals are essential micronutrients for most living beings, including bacteria. In addition, they play important roles at the host-pathogen interface: the host tends to restrict bacterial access to iron, manganese and zinc, while intoxicating invading microorganisms with copper or zinc during phagocytosis. Bacteria have therefore acquired various homeostasis mechanisms in order to adapt to those conditions. Whereas iron, zinc or manganese import systems have been extensively characterized, very little is known for copper, for which studies have mostly focused on defense mechanisms. Besides, while several post-transcriptional regulation mechanisms are known for other metals, only transcriptional regulators have been identified in response to copper.Previous work performed in the laboratory on copper homeostasis in the human-restricted pathogen Bordetella pertussis, responsible for the whooping cough disease, has shown that this bacterium has shed most of its defense mechanisms against excess copper. On the other hand, we have identified a three-gene operon called bp2923-bfrG-bp2921, in which the last two genes are down-regulated by copper excess. bfrG is notably predicted to encode a TonB-dependent transporter, a protein family well-known for metal import across the outer membrane in Gram-negative bacteria, and bp2921 has a characterized homolog encoding a siderophore reductase, which hints at a system involved in copper acquisition. We have shown that the protein encoded by the first gene, a member of the DUF2946 protein family, represents a new type of upstream Open Reading Frame (uORF) involved in post-transcriptional regulation of the downstream genes. In the absence of copper, the entire operon is transcribed and translated. Perception of copper by the nascent bp2923-coded protein via its conserved CXXC motif triggers Rho-dependent transcription termination between the first and second genes by relieving translation arrest on a conserved C-terminal RAPP motif. Homologs of bp2923 are widespread in bacterial genomes, where they head operons predicted to participate in copper importation or utilization. We have thus identified a new mode of genetic regulation by a transition metal and identified a regulatory function for a member of an uncharacterized family of bacterial proteins that we have named CruR, for Copper responsive upstream Regulator. Additional work on this system has shed a light on the complexity of bacterial regulation, as our operon is regulated not only by copper, but is also overexpressed upon virulence modulation or in stationary growth phase.We have also initiated the characterization of the function of this operon. BfrG has been shown to specifically bind copper in vitro, and phenotypic analyses have shown a crucial role for the operon when B. pertussis is placed in low-oxygen conditions. Among the cuproproteins produced by B. pertussis are several cytochrome oxidases in the respiratory chain, which suggests that BfrG and Bp2921 could play a role in delivering copper for their assembly. Combined with results on the regulation, this suggests a possible role for copper and our operon in bacterial persistence in the respiratory tract during infection. Many aspects of this system remain to be further investigated
Duc, Céline. "Identification des génes impliqués dans la signalisation du statut en fer chez les végétaux." Montpellier SupAgro, 2009. http://www.theses.fr/2009NSAM0018.
Повний текст джерелаDevergnas, Séverine. "Etude et caractérisation de l'expression de nouveaux transporteurs de zinc de la famille ZnT chez les mammifères." Université Joseph Fourier (Grenoble), 2005. http://www.theses.fr/2005GRE10237.
Повний текст джерелаZinc is an essential trace element. It is involved in many cellular processes because it is a cofactor of enzymes, nuc1ear factors and hormones. Therefore, is a very important component of cell viability Zinc homeostasis results from a coordinated regulation of different proteins: ZIP (uptake), metallothioneins (intracellular storage/trafficking), and ZnT (excretion). Using genomic databanks, we have analyzed and identified two novel SLC30 genes: SLC30A8 and SLC30A10. Zinc homeostasis is maintained by the action of these proteins, and their transcription is partly dependent of extra cellular zinc concentration. Ln case of zinc deficiency, ZnT-5, -5c and -7 genes are over-expressed. These transporters that we have localized in the Golgi apparatus could provide essential zinc to neo-synthesised proteins for their functionality. Furthermore, we showed that ZnT-8 is a zinc transporter specifie of pancreas and expressed in beta cells. ZnT -8 facilitates the accumulation of zinc from the cytoplasm into insulin vesic1es, and its transcription regulation is dependent, like insulin, of extra cellular glucose concentration. Zinc is implicated in all metabolic and structural aspects of the different cellular compartments. Therefore the cellular control of Zinc requires to be understood and is essential tot fear the cellular working
Chaste, Pauline. "Exploration de deux processus associés à l'autisme : la synaptogénèse et la signalisation de la mélatonine." Paris 7, 2010. http://www.theses.fr/2010PA077126.
Повний текст джерелаThe search for rare mutations or chromosomal rearrangements, has recently allowed new hypotheses regarding the genetic mechanisms involved in autism. Previous studies in the laboratory have allowed to show mutations of neuroligins 3 and 4, which encode neuronal cell adhesion molecules. My thesis was in the continuity of this work, pursuing a strategy of search of rare mutations in candidate genes. I studied the one hand MAGI2 gene, which encodes a partner of neuroligins, in 96 subjects with autism. On the other hand, I studied genes of the melatonin pathway in patients with autism, and ADHD subjects, to clarify the mechanisms and specificity of alterations of this pathway. Also my work has included clinical reevaluation of patients who carried mutations of SHANK3. The study of MAGI2 and SHANK3 genes showed that mutations in neuroligins partners may have a role in the emergence of an "isolated" autistic syndrome. However, the gene MAGI2 does not seem particularly involved in autism, and may be associated with a more severe phenotype. The study of the melatonin pathway confïrms the likely preponderance of a deficit of melatonin synthesis as a mechanism for alteration of this pathway in autism and that alteration of this pathway is not specific to autism. Finally, the two processes explored in this thesis could play a role in a common process; the maintenance of synaptic homeostasis