Contents
Academic literature on the topic 'Récepteurs au C3b du complément'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Récepteurs au C3b du complément.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Récepteurs au C3b du complément"
Deveuve, Quentin, Valérie Gouilleux-Gruart, Gilles Thibault, and Laurie Lajoie. "La région charnière des anticorps thérapeutiques." médecine/sciences 35, no. 12 (December 2019): 1098–105. http://dx.doi.org/10.1051/medsci/2019218.
Full textVecchierini, Marie-Françoise. "Traitement médical des troubles respiratoires obstructifs du sommeil de l’enfant et de l’adolescent." L'Orthodontie Française 90, no. 3-4 (September 2019): 311–20. http://dx.doi.org/10.1051/orthodfr/2019027.
Full textDissertations / Theses on the topic "Récepteurs au C3b du complément"
Kisserli, Aymric. "Distribution, rôle et régulation du CRI (CD35, récepteur pour le C3b/C4b) érythrocytaire. Analyse de dépôts érythrocytaires de fractions du complément." Reims, 2008. http://theses.univ-reims.fr/exl-doc/GED00000886.pdf.
Full text@CR1 (CD35, the C3b/C4b receptor) is a transmembrane glycoprotein found on few cell types. Erythrocyte CR1 (E-CR1) is involved in immune complex (IC) clearance in liver and spleen. The binding of IC on E is improved by cluster distribution of CR1 enabling a strong avidity multivalent binding. Rhesus macaque (Macaca mulatta) was shown to express a transmembrane E-CR1 as observed in Human (same length, density, cluster distribution). This “human-type” CR1 was characterized by allotypic polymorphisms. A shorter CR1 was also observed, called CR1like (CR1L) which was more abundant, more diffuse and glycophosphatidylinositol anchored. Polymorphisms of CR1 Sla region involved in rosetting between healthy E and P. Falciparum infected E were described in 12 primate species. E from rhesus macaque were not prevented from rosetting with human infected E by those polymorphisms. CR1 and CR1L promoters from rhesus macaque (MCR1, MCR1L) were sequenced. AML1 known as human CR1 activator was found in MCR1 but was missing in MCR1L. Ets and MZF1 were conserved. HES1 et LBP1 might downregulate MCR1 and human CR1L. An allelic polymorphism corresponding to a 18 nucleotide deletion was observed in human CR1L promoter. C4d deposition at E surface (EC4d) of patients suffering from kidney acute humoral rejection was compared with biopsy analysis and related to C4d tissue deposits. EC4d appears a promising non-invasive marker of acute humoral rejection. The mechanism of C4d deposition remains to be investigated. Complement classical pathway activation did not seem to be involved
Devaux, Patricia. "Une molécule CD46 et deux fonctions : récepteur du virus de la rougeole et régulateur de l'activation du complément." Paris 7, 1998. http://www.theses.fr/1998PA077036.
Full textBénard, Magalie. "Étude du rôle des récepteurs des anaphylatoxines C3a et C5a dans le remodelage et le développement tissulaires." Rouen, 2007. http://www.theses.fr/2007ROUES013.
Full textComplement anaphylatoxines and their receptors, C3Ar and C5aR, play a role in regeneration and ontogenesis. Hepatocytes express C5aR only after inflammatory stress. C5a administration increase the hepatocyte proliferation in vitro and in vivo, during liver generation. C3aR and C5aR are expressed in granular neurons of rat cerebellum during development. In vitro, C5aR protects granular neurons against apoptosis induced by lack of substract in medium ; in vivo, sub-dural injection of C5a induces an increase of neuroblast proliferation by a direct action of this peptide on C5aR. C3a injection provokes a decrease of cerebellar external layer and a concomitant increase of internal layer that could be explained by an acceleration of granular neuron migration as measured in vitro by an increase of neuroblast motility
Sayah, Sakina. "Implication du complément dans les mécanismes inflammatoires du système nerveux central : expression des récepteurs des anaphylatoxines C3a (C3aR) et C5a (C5aR) par les astrocytes." Rouen, 1998. http://www.theses.fr/1998ROUES081.
Full textThorel, Nathalie. "Rôle du complément dans la réaction inflammatoire gliale : contribution à l'étude du CR2/CD21 et du GPR176." Rouen, 2009. http://www.theses.fr/2009ROUES041.
Full textIn order to decipher the function of anaphylatoxins in the central nervous system, we stimulated glioblastomas cells with C3a which leads us to the discovery of two molecules induced by C3a. CR2 is expressed on astrocytes but its function is unknown. We produced a monoclonal antibody which can activate astrocytic CR2 which translocates with TAPA-1 and with the non-muscle caldesmon. These proteins are known to arrest cell migration. In a second part, we study the GPR176 whose ligand is unknown. We immunized rabbits and mice with four protocols but we failed to obtain an antibody. We localized GPR176 in the central nervous system and particularly in the lombar spinal cord and in locus coeruleus. We produced a stable cell line which will be used in ligand finding. These results don't show an interaction between the complex TAPA-1/CR2 and GPR176 with glial inflammation but findings obtained with CR2 suppose a role of this receptor in promoting glial scar formation
Mahmoudi, Abd-elrachid. "Etude génotypique et phénotypique des polymorphismes du récepteur du complément de type 1 (CR1,CD35) dans la maladie d’Alzheimer." Thesis, Reims, 2015. http://www.theses.fr/2015REIMM201/document.
Full textGenome-wide association studies have identified new loci, including the CR1 gene, as being associated with Alzheimer's disease (AD) risk. The complement receptor type 1 (CR1) is a transmembrane glycoprotein found on the surface of erythrocytes (CR1E), and also in the plasma in soluble form (CR1s). CR1 can have different functional forms that may confer different risk levels, or even suggest pathophysiological mechanisms of AD. Indeed, the relation between CR1 and AD is now well established, the mechanism of this association remains to be elucidated.The main objective of this thesis was to correlate acquired phenotype elements, such as density of CR1E (number of CR1 antigenic sites per erythrocyte) or CR1s with genetic data (single nucleotide polymorphisms, length and density polymorphisms). Firstly, our study showed using two different methods that AD is associated with low density of the long CR1 isoform (CR1*2) and suggested the possible existence of silent CR1 alleles. Secondly, we showed that although genetic criteria were met, some phenotypes could be acquired during the course of the disease. Our findings suggest that AD stems more from insufficient clearance of amyloid deposits than from excessive response whose inflammatory reaction might be deleterious. Although this genetic and phenotypic study with pathophysiological potential still require further investigation on a larger scale, she could pave the way towards new therapeutic avenues that currently remain elusive in the absence of a clear overview of the mechanisms involved
Rey-Millet, Macary Catherine. "Association covalente antigène-protéine C3b du complément : rôle dans l'apprêtement intracellulaire de l'antigène." Grenoble 1, 1993. http://www.theses.fr/1993GRE10212.
Full textChaumonnot, Killian. "La protéine de choc thermique Gp96 dans les macrophages au cours du stress du RE : Interaction avec le complément C3." Thesis, Bourgogne Franche-Comté, 2020. http://www.theses.fr/2020UBFCJ002.
Full textThe stress protein Gp96, is an endoplasmic reticulum (ER) protein of the HSP90 family, expressed in all cells. Under ER stress, it is induced and can then be expressed at the membrane and extracellular levels. Gp96 is known to have a dual role in immune responses, having both pro- and anti-inflammatory effects. Although it has been shown to be necessary for the tolerance of intestinal macrophages to the microbiota, its role has not been elucidated at the molecular level. Moreover, its effects in macrophages under ER stress are not known, despite their involvement in many pathologies. In this work, we first show that Gp96 is expressed at the membrane of M2 and not M1 macrophages derived from blood monocytes of healthy volunteers. We show that ER stress, generated by the disruption of calcium homeostasis induced by thapsigargine (Tg), results in a switch from the M2 phenotype to a functional Gp96-dependent pro-inflammatory profile. This switch is associated with the decrease in membrane expression of Gp96 and its secretion. In a second step, we demonstrate that Gp96 interacts with intracellular complement C3 in macrophages M1 and M2. This interaction is more important in stressed M2 macrophages than in untreated M2 and, C3b, the fragment resulting from the cleavage of C3, is present only in the culture supernatant of the stressed M2, and could moreover be co-immunoprecipitated with Gp96. Finally, like Gp96, the inactivated fragment of C3b, iC3b, is detected only at the membrane of unstressed M2 and its presence is dependent on functional Gp96. These results suggest that membrane Gp96 and iC3b could be markers of anti-inflammatory M2 macrophages. They show that Gp96 is involved in the modulation of the M2 phenotype towards a pro-inflammatory profile induced by a disruption of calcium homeostasis. This effect could be related to its ability to interact with the C3 complement whose C3a and C3b cleavage fragments have pro-inflammatory effects
Poursharifi, Pegah. "Immunometabolic aspect of C5L2 and C5aR in adiposity : physical, functional and physiological interactions." Doctoral thesis, Université Laval, 2014. http://hdl.handle.net/20.500.11794/25593.
Full textFrom the convergence of metabolism and immune research has emerged a new research field, termed “Immunometabolism”. Obesity, an immunometabolic disease, is associated with a state of low-grade inflammation and is characterized by increased infiltration of macrophages into adipose tissue. Complement activation can act as an early trigger and precursor of other immune functions. C5aR-like receptor 2 (C5L2) has been identified as a receptor for Acylation Stimulating Protein (ASP) and the inflammatory factor C5a (which can also bind C5aR). This thesis sequentially evaluates (i) ligand-induced C5L2 and C5aR interaction in cultured 3T3-L1 adipocytes and J774 macrophages, (ii) the C5aR contribution in adipocyte metabolic and immune responses in mouse models, (iii) as well as C5L2 and C5aR association with obesity-related factors in humans. The immunometabolic receptors, C5L2 and C5aR, constitutively self-associate into homo-/heterodimers and ligand treatment of 3T3-L1 adipocytes and J774 macrophages increased their colocalization. Both C5a and ASP directly induced primary adipocyte signaling and function. However, in C5aRKO primary adipocytes, C5a effects were disrupted, while stimulatory effects of ASP were mostly maintained. Moreover, addition of C5a completely blocked ASP signaling and activity in both C5aRKO and WT primary adipocytes. Finally, C5L2 and C5aR expression in adipose tissue from morbidly obese women was associated with increased adiposity. Interestingly, ASP/C5L2 and C5L2/C5aR ratio markedly increased with abdominal obesity. Taken together, the closely linked physical, functional and physiological interaction between C5L2 and C5aR in adipocytes suggests a potential role in adipose tissue immunometabolism. This further highlights the important new links between adipose tissue and complement proteins/receptors and demonstrates how excessive immunometabolic responses may exacerbate adiposity.
Blanc, Caroline. "Etude des auto-anticorps anti-Facteur H dans le Syndrome Hémolytique et Urémique atypique et dans la glomérulonéphrites membrano-prolifératives." Paris 7, 2012. http://www.theses.fr/2012PA077003.
Full textDysregulation of the complement System is linked to two different renal diseases: aHUS and MPGN The autoimmune form of aHUS is due to generation of autoantibodies directed Factor H. Moreover, we have characterized anti-FH IgG in patients presenting with MPGN. AI-aHUS patients had increased levels of FH-containing immune complexes and perturbation of FH-dependent cell-protection, in contrast to MPGN patients. AI-aHUS associated antibodies bound both N-and C-terminal domains of FH, while in case of AI-MPGN they bound the FH N-terminal domain only. The homozygous deletion of Factor H related protein CFHR1 is strongly associated with AI-aHUS and may play a role in the underlying mechanisms of anti-FH autoantibodies generation and in their pathological role. An in silico prediction of the epitopes potentially presented by the HLA-A24 was conducted and revealed a high sequence similarity between FH-derived peptides and peptides of a parasitic origin, correlated with the analysis of the clinical and biological symptoms of the AI-aHUS. Taken together, these results suggested that the mechanisms underlying the auto-immunization are related to a loss of tolerance due to a deletion of a FH homologous gene and a cross-reactivity towards a parasite antigen in AI-aHUS. In MPGN, anti-FH antibodies are frequently associated to monoclonal gammopathy or with other autoantibodies, directed against and stabilizing the C3 convertase, therefore revealing more heterogeneous mechanisms of immunization. These results led to a better understanding of the pathophysiological differencies between aHUS and MPGN. They could also reveal new auto-immunization scenario in autoimmune diseases