Tesis sobre el tema "Lupus érythémateus aigu disséminé"
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Jouan, Dominique. "Les manifestations ophtalmologiques du lupus érhytémateux aigu disséminé". Caen, 1990. http://www.theses.fr/1990CAEN3075.
Texto completoTrebeden-Negre, Hélène. "Modulation de la réponse auto-immune et anti-tumorale par l'injection de cellules apoptotiques". Paris 5, 2002. http://www.theses.fr/2002PA05N079.
Texto completoWe investigated whether the increased rate of lymphocyte apoptosis in systemic lupus erythematosus can trigger the onset of the disease. Only injection of apoptotic B cells accelerates the onset of the lupus. We observe an increase in the Th2 response directed against the histone H2A after injection of apoptotic B cells. This phenomenon can be explained by a preferential expression of the histone H2A by B cells and the histone H3 by T cells. We also analysed tumor cells apoptosis implication in the anti-tumoral immune response. Injection of two million apoptotic cells to BALB / c mice induces a Th2 antiinflammatory response through complement dependent cytotoxicity
Nathou, Marie-Odile. "Le lupus érythemateux disséminé en Guadeloupe : étude rétrospective à propos de 81 cas". Bordeaux 2, 1995. http://www.theses.fr/1995BOR2M030.
Texto completoGRE, JEROME. "Le lupus erythemateux dissemine familial : a partir de deux observations cliniques". Bordeaux 2, 1988. http://www.theses.fr/1988BOR25151.
Texto completoChazal, Jean-Louis. "Manisfestations neuro-psychiques du lupus érythémateux disséminé : à propos d' une observation". Clermont-Ferrand 1, 1987. http://www.theses.fr/1987CLF11032.
Texto completoJanah, Taoufik. "Sur quelques modes de réponses psychologiques et psychopathologiques à la maladie organique chronique chez l'adulte : cas du lupus érythémateux disséminé systémique (la maladie lupique) : esquisse d'une approche somatopsychologique". Paris 13, 1993. http://www.theses.fr/1993PA131032.
Texto completoMeillon, Paul. "La myélofibrose au cours du lupus érythémateux aigu disséminé : à propos d'un cas". Bordeaux 2, 1996. http://www.theses.fr/1996BOR2M018.
Texto completoBoisvert, Jean. "Lupus et pancréatites : à propos de trois observations". Bordeaux 2, 1995. http://www.theses.fr/1995BOR2M078.
Texto completoPlantin-Carrenard, Emmanuelle. "Thalidomide et lupus érythémateux cutanés". Paris 5, 1996. http://www.theses.fr/1996PA05P113.
Texto completoSchickel, Jean-Nicolas. "Lupus érythémateux disséminé et sous-expression de Carabin et Sh3kbp1 : étude par génomique fonctionnelle". Strasbourg, 2011. https://publication-theses.unistra.fr/public/theses_doctorat/2011/SCHICKEL_Jean-Nicolas_2011_ED414.pdf.
Texto completo(Carabin) and SH3KBP1. The aim of this thesis project was to precise the consequences of Carabin and Sh3kbp1 underexpression in B cell function and in the development of autoimmunity. To address those issues, we produced: 1/ Carabin and Sh3kbp1 knock-down (KD) B cells and studied their phenotype; 2) a knock-out (KO) and conditional KO of Carabin in B cells or in mature B or T cells. Our results show that Carabin deficiency leads to an increase in T and B cell activation after TCR and BCR stimulation, respectively. Moreover Carabin KO mice and B cell conditional KO mice shows an accelerated T-dependant and T-independent antigen-specific B cell response in vivo. Finally, Carabin KO mice develop signs of autoimmunity after CpG treatment characterized by sustained production of anti-DNA IgG as well as an important deposition of IgG in renal glomeruli. Altogether these results define a new role for Carabin as a negative regulator of B cell signaling that points out a new defective biological pathway in autoimmunity. For Sh3kbp1, we show an acceleration of Erk and Akt phosphorylation in Sh3kbp1 KD B cells after BCR engagement, showing a role for Sh3kbp1 as a negative regulator of B cell receptor signaling. In conclusion, we have identified two genes that are deregulated in B cells during SLE. A deficiency in one of these two genes speed up the B cells response and predispose for the development of autoimmunity in vivo. Further experiments could potentially identify these two genes as new susceptibility genes in SLE
Villaret, Eric. "Maladie lupique et hormones sexuelles : aspects biologiques et thérapeutiques". Bordeaux 2, 1988. http://www.theses.fr/1988BOR25338.
Texto completoBiron-Andréani, Christine. "Etude de la spécificité des auto-anticorps antiphospholipides dans le lupus erythemateux disséminé". Bordeaux 2, 1992. http://www.theses.fr/1992BOR23080.
Texto completoLaporte, Catherine. "Approche congénique de la prédisposition au lupus érythémateux disséminé chez la souris New Zealand White". Aix-Marseille 2, 2003. http://www.theses.fr/2003AIX22017.
Texto completoCardineau, Érick. "Néphropathies lupiques : à propos de 18 observations". Caen, 1991. http://www.theses.fr/1991CAEN3031.
Texto completoBonardel, Gérald. "Les manifestations cardiovasculaires au cours du lupus érythémateux disséminé : à propos de 42 observations". Bordeaux 2, 1994. http://www.theses.fr/1994BOR2M082.
Texto completoLajaunias, Frédéric. "Rôle de CD22 et son ligand dans le lupus érythémateux disséminé". Paris 7, 2002. http://www.theses.fr/2002PA077214.
Texto completoMénétrier-Caux, Christine. "Production d'anticorps monoclonaux dirigés contre les leucocytes de chien : étude du lupus érythémateux disséminé (LED) canin". Lyon 1, 1992. http://www.theses.fr/1992LYO1T112.
Texto completoIng, Heangrek. "Les paralysies oculo-motrices au cours d'un lupus érythémateux". Montpellier 1, 1988. http://www.theses.fr/1988MON11041.
Texto completoLacotte, Stéphanie. "Comprendre, cibler et éliminer les lymphocytes B autoréactifs au cours du lupus : vers une application thérapeutique des nanotubes de carbone comme vecteurs de peptides bioactifs". Strasbourg, 2009. http://www.theses.fr/2009STRA6019.
Texto completoSystemic lupus erythematosus is considered as a B cells disease. Therefore, we decided to design an therapeutic strategy aiming at specifically suppressing pathogenic autoreactive B lymphocytes. This strategy is based on the use of carbon nanotubes in order to deliver two types of molecules: one is a peptide derived from a major lupus autoantigen and will allow us to target B cells to be eliminated via their antigen surface receptor; the other one will harbor a proapoptotic activity, leading to cell death. The use of functionalized carbon nanotube as carrier has been validated because of their absence of effect on immune cells in vitro. The Nterminal region of histone H2B represents a preferential target for autoantibodies in lupus mice and is implicated in the development of lupus pathology. It will be the target molecule. I could highlight CXCR3expressing, pathogen IgGproducing plasma cell population that can migrate in the inflamed kidneys where they can contribute to lesions
Yougbare, Issaka. "Rôle de la phosphodiestérase spécifique de l'AMPc (PDE4) dans deux modèles d'inflammation chronique : le lupus érythémateux disséminé et l'asthme". Strasbourg, 2010. https://publication-theses.unistra.fr/public/theses_doctorat/2010/YOUGBARE_Issaka_2010.pdf.
Texto completoChronic inflammation is a deleterious process which occurs in several pathologies such as the autoimmune diseases and the recurrent pulmonary diseases. It causes in the long term tissue damage and the concerned organ dysfunction. The phosphodiesterases which specifically hydrolyze cAMP, like PDE4 isozymes, are believed to be involved in the control of the inflammatory response. Indeed, the inflammation is strongly correlated to low intracellular cAMP level which results from an increase in PDE hydrolytic activities. We hypothesize that chronic inflammatory diseases (such as lupus and asthma) would be associated toPDE4 signaling alterations. The goal of this work is to investigate the role of PDE4 and the consequences of their inhibition in the chronic inflammation. Thus for the enzymatic activities, the pharmaco-mechanical and biochemical properties which are likely modulated by a rise in intracellular cAMP following the inhibition of PDE4 were analyzed. In the murine lupic model, we showed that the disease progression is correlated with an increase in PDE4 activity. This change of PDE4 hydrolytic activity in the MRL/lpr lupus- prone mouse kidney is associated with alterations in PDE4 expression (4A, 4B, 4C and 4D). Among the three PDE4 inhibitors (pentoxifylline, Denbufylline and NSC613) administrated to lupus-prone mice, only the NCS 613 significantly increases the survival of the treated animals while delaying the production of the auto-antibodies, the proteinuria and the secretion of TNFα. We also showed that the chronic treatment with NCS 613 increases the cAMP level in the kidney, which is strongly correlated to a lower inflammation status in this tissue. Moreover, this treatment reversed changes in PDE4 expression level observed during the lupus disease progression. In human lung parenchyma, we have characterized a high PDE4 activity as well as the expression of the four PDE4 isoenzymes in the cytosolic, microsomal and nuclear fractions. Functional studies demonstrated that NCS 613 prevented huaman bronchial hyperresponsiveness resulting from the inflammation induced in vitro. Moreover, the NCS 613 decreases mechanical tensions induced by three independent agonists (methacholine, histamine and U-46619) in TNFα-treated bronchi. NCS 613 also decreases inflammation markers by increasing kidney cAMP level of the lupic mice and by protecting IBα degradation in cultured pulmonary parenchyma. NCS 613 exerts its anti-inflammatory effect by inhibiting phospho-p38 MAPK and NFB pathways in PBMC from lupic patient and A549 cell line. The results of this work confirm that PDE4 are directly involved in chronic inflammations (lupus and asthma) and that their inhibition could constitute an alternative therapeutic strategy to corticosteroids. NCS 613 is a novel PDE4 inhibitor which exerts its anti-inflammatory effect at the systemic, tissue and subcellular levels. Its use would be potentially beneficial for the treatment of the lupus and asthma due to the fact that contrary to other PDE4 inhibitors NCS 613 has basically no emetic effect
Bourges, Monique. "Endocardites de Libman-Sacks : à propos d'un cas - revue de la littérature". Bordeaux 2, 1992. http://www.theses.fr/1992BOR2M114.
Texto completoMariacher, Carine. "Le lupus érythémateux : une observation pédiatrique". Paris 5, 1994. http://www.theses.fr/1994PA05P024.
Texto completoBroustet, Henri. "Les manifestations neuropsychiatriques au cours du lupus erythémateux disséminé : à propos de 19 cas". Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M166.
Texto completoRichez, Christophe. "Sécrétion inappropriée d'interferon-alpha par les cellules dendritiques au cours du Lupus erythemateux systémique". Bordeaux 2, 2009. http://www.theses.fr/2009BOR21624.
Texto completoPage, Nicolas. "Etude du mécanisme d'action du phosphopeptide P140 : un modulateur de la réponse autoimmune dans le lupus". Strasbourg, 2010. http://www.theses.fr/2010STRA6235.
Texto completoSystemic lupus erythematosous is an inflammatory chronic disease characterized by the loss of self tolerance and autoreactive B lymphocytes hyperprolifération, which lead to autoantibodies production. These autoantibodies participate to the formation of immune complexes, which are responsible for the dysfunction of different organs, whose kidneys are the most frequently affected. Nowadays, most strategies used in lupus treatment consist in an overall immunosuppression, which is often associated with undesirable side effects. To work out this problem, our laboratory developed a tolerogenic peptide, called P140, immunomodulating the autoimmune response and delaying the appearance of symptoms in lupus-prone MRL/lpr mice, without weakening the overall immune response. This peptide, corresponding to the 131-151 sequence of the U1-70K spliceosomal protein, is phosphorylated on Ser140 residue. Phase IIa and IIb clinical trials have given promising results and a phase III is planned. In order to determine the process underlying the impairment of the autoimmune response in the presence of P140 peptide, we analyzed along this work the cellular and molecular mechanisms affected by this peptide. Thanks to a proteomic analysis, we identified the heat shock protein HSC70 as a single and unexpected receptor for P140 peptide. Then, the beneficial effect of the peptide was examined at two different levels. First, we carried out a structure-function study with different P140 peptide analogues toward HSC70, and we analyzed the functional impact of the peptide on HSC70-containing protein complexes, especially by studying the expression/stability of MHC II molecules and some co-chaperones. Then, we found that, following binding to HSC70, P140 peptide induces a decrease of peripheral hypercellularity in MRL/lpr mice, consequent to the inactivation of the Fas apoptotic pathway in these mice. To explain this regulation of cellular homeostasis mediated by P140 peptide, we proposed two different mechanisms. The first one involves cytotoxic γδ T cells, a particular T cell subpopulation known for its reactivity toward phosphorylated ligands, and the second one supporting an inhibitory role for P140 peptide on peptide presentation via MHC II molecules
Augias, Didier. "Le lupus cutané subaigu : une entité ?" Montpellier 1, 1996. http://www.theses.fr/1996MON11018.
Texto completoRiemens, Dominique Annie. "Manifestations neuropsychiatriques du lupus érythémateux disséminé : à propos de 27 observations à l'île de la Réunion". Bordeaux 2, 1989. http://www.theses.fr/1989BOR25035.
Texto completoSaussaye, Yannick. "Mucinose dermique et lupus : à propos d'un cas avec revue de la littérature". Montpellier 1, 1994. http://www.theses.fr/1994MON11161.
Texto completoJouffret-Faure, Isabelle. "Troubles neuro-psychiatriques dans le lupus érythémateux disséminé de la personne âgée : à propos d'un cas. Revue de la littérature". Montpellier 1, 1994. http://www.theses.fr/1994MON11120.
Texto completoTomasetig, Evelyne. "Lupus erythemateux aigu disséminé et enteropathie exsudative : à propos de deux cas, revue de la littérature". Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M209.
Texto completoResplandy, François. "Etude des auto-anticorps anti-cellule endothéliale et exploration biologique de l'endothelium dans le lupus érythémateux disséminé". Bordeaux 2, 2000. http://www.theses.fr/2000BOR2P022.
Texto completoDupuy, Rémy. "Anticorps anti-cellules endothéliales et marqueurs solubles de dysfonction endothéliale au cours du lupus érythémateux disséminé". Bordeaux 2, 1998. http://www.theses.fr/1998BOR23037.
Texto completoBrun, Susana. "Quel rôle pour l'IL-21 dans la maladie lupique ? : étude de la différenciation plasmocytaire". Strasbourg, 2011. http://www.theses.fr/2011STRA6109.
Texto completoSystemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by B cell hyperactivity leading to the production of autoantibodies, some of which have a deleterious effect. Recently, IL-21 was shown to play a key role in the differentiation of B cells into plasma cells (PC) in a non-autoimmune context. But what about its role in the progression of lupus disease? This was the aim of my thesis project, which consisted in studying the role of IL-21 in PC differentiation in this autoimmune setting. For that purpose, we chose to work with NZB/W female mice, which spontaneously develop a disease similar to human SLE. Our results show an increase in serum IL-21 levels and in the expression of IL-21 receptor by B cells during SLE development. In addition, NZB/W B cells appear to be more sensitive to the signal induced by IL-21, which leads to increased IgG production. We also observed expansion of a T cell subset, which is one of the main sources of IL-21 within the germinal centers, i. E. Follicular helper T cells. Our data seem to confirm the involvement of IL-21 in the B cell response in SLE. In order to analyze plasma cell differentiation in a pathophysiological context, we also set up B cells / CD4+ T cells co-culture experiments using cells isolated from NZB/W mice harboring different stages of the disease. These experiments allowed us to identify two populations in vitro, one which may correspond to PC (B220lowCD138hi) and the other one which may be plasmablasts (B220+CD138int). The differentiation of the latter population is affected when the interaction of IL-21 with its receptor is blocked
Kotovskaya, Maria. "Identification et intérêt physiopathologique de nouveaux biomarqueurs dans les formes précoces et neurologiques de lupus érythémateux disséminé : Potentiel diagnostic et thérapeutique". Université Louis Pasteur (Strasbourg) (1971-2008), 2008. http://www.theses.fr/2008STR13101.
Texto completoOne of the features of systemic lupus erythematosus (SLE) is the production of potentially pathogenic autoantibodies, directed against a wide variety of autoantigens, mainly nuclear. In our study, we focused on the production of autoantibodies in two different forms of SLE. First, we analyzed the humoral response of untreated lupus patients, i. E. In the very early phase of clinical development of the disease. We also studied the neurological forms of lupus - the most disabling ones - which can be life-threatening. We were also committed to identify the autoantigens recognized by the autoantibodies circulating in the serum of patients with neurological lupus. The strategy we have developed is very promising and could be used on other neurological and autoimmune diseases
Portecop, Patrick. "Endocardite de Libman-Sacks, à propos d'un cas". Bordeaux 2, 1998. http://www.theses.fr/1998BOR2M023.
Texto completoBesson-Léaud, Laurent. "Lupus néonatal". Bordeaux 2, 1997. http://www.theses.fr/1997BOR23079.
Texto completoWawrezinieck, Anne. "Elaboration d'un vecteur pharmaceutique complexe pour l'administration par voie orale d'un peptide protecteur contre le lupus érythémateux disséminé". Université Louis Pasteur (Strasbourg) (1971-2008), 2007. http://www.theses.fr/2007STR13240.
Texto completoBlanco, Patrick. "Rôle des cellules dendritiques et des lymphocytes T CD8+ dans la physiopathologie du lupus érythémateux systémique". Bordeaux 2, 2004. http://www.theses.fr/2004BOR21183.
Texto completoSystemic lupus erythematosus (SLE) represents a model for systemic autoimmune diseases. SLE pathogenesis remains unknown but involves environmental, genetic and immunological factors. The aim of the present study was to investigate the role of dendritic cells (DC) and CD8+ T-lymphocytes in the pathogenesis of the disease. We show that human SLE patients are characterized by an activation of the DCs system mediated by an unabated secretion of alpha-interferon by plasmacytoid DCs. In addition the activation of the DC system accounts for an activation of the CD8+ T-cell compartment. Those CD8+ T-lymphocytes are able to generate in vitro high amount of soluble nucleosome and unique fragment of autoantigen. Moreover myelin autoreactive CD8+ T-lymphocytes are present in neuropsychiatric SLE patients with white matter lesions. Taken together those results bring new elements in the comprehension of SLE pathogenesis as well as new immunotherapeutic targets
Marck, Yves. "Le syndrome des anticorps antiphospholipides : revue de la littérature à propos d'un cas". Montpellier 1, 1992. http://www.theses.fr/1992MON11060.
Texto completoDistinguin, Sophie. "Lupus induit au Rimifon : à propos d'un cas, revue de la littérature". Bordeaux 2, 1995. http://www.theses.fr/1995BOR2M039.
Texto completoBessis, Didier. "Thalidomide et maladie lupique : intérêt du thalidomide dans le traitement du lupus systémique". Montpellier 1, 1991. http://www.theses.fr/1991MON11188.
Texto completoLaunay, David. "Identification et caractérisation moléculaire des cibles antigéniques dans les manifestations neurologiques centrales du lupus systémique". Lille 2, 2008. http://www.theses.fr/2008LIL2S012.
Texto completoGuillet, Stéphanie. "Monogenic predisposition to systemic lupus erythematosus and efferocytosis Impaired efferocytosis and Systemic Lupus Erythematosus in patients with autosomal recessive ACK1 and BRK Kinases deficiencies". Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB003.
Texto completoSystemic Lupus Erythematosus (SLE) is a collection of autoimmune diseases characterized by auto-antibodies against nuclear antigens. Pathogenesis of SLE remains unclear and disease mechanisms may be multiple. Here we report the identification of autosomal recessive loss-of-function variants in the kinase domain of ACK1 and BRK, in patients from two families with SLE. Using patients and controls iPSC-derived Tim4+ resident-like macrophages we find that wild-type ACK1 and BRK are dispensable for phagocytosis of bacteria and fungi, but are both required for efficient efferocytosis, including actin-mediated engulfment of apoptotic cells by human macrophages, and an early cell-autonomous anti-inflammatory gene expression program driven by AKT and STAT3 and triggered by apoptotic cells. These results indicate that ACK1 and BRK kinases activity are required for the immunologically silent clearance of apoptotic cells by macrophages and define genetic efferocytosis deficiency in a subset of SLE patients who may benefit from personalized therapy in the future
Lemoine, Sébastien. "Étude du rôle du lymphocyte B dans la tolérance périphérique". Brest, 2011. http://www.theses.fr/2011BRES2308.
Texto completoNature has provided the immune system with numerous checkpoints controlling the maintenance of tolerance and the prevention of autoimmunity. The regulatory mechanisms operating in the periphery of the immune system are mediated mainly by a specific population of regulatory T cells considered as the main contributor to peripheral tolerance. In auto immunity, B cells are generally considered pathogenic since they release autoantibodies, that can cause damages to target tissues. However B cell depletion in several murine models of autoimmune diseases leads to a more severe pathology, giving B cells an unexpected regulatory role. Insights have been realized concerning the mechanism of action and the phenotype of this particular subset of regulatory B cells in mice and two subsets of IL-10 secreting B cells have been endowed with regulatory properties. However, despite increasing interest in regulatory B cell biology, the existence of an equivalent population in human is still a matter of controversy. The current study indicates that activated T cells can induce their own regulation by promoting the development of a B-cell dependent regulatory process. Regulatory B cells, identified by their expression of CD19high IgD+ CD24high CD38high CD5high, inhibit the proliferation and cytokine secretion of proinflammatory TH1 cells with the contribution of regulatory T cells, placing B cells at the center of immunosuppressive reactions. The assessment of this new regulatory function in autoimmune diseases shows that B-cell mediated immune regulation is deficient in Systemic Lupus Erythematosus
Bensaada, Souad. "Etude de l'effet perturbateur endocrinien d'isoflavones végétales, approches clinique et mécanistique. Réduction de ces substances dans l'alimentation humaine". Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0109.
Texto completoThe consumption of soy, a valuable source of plant-based protein, has seen a steady rise in France. However, soy contains isoflavones (IFs) which are phytoestrogens with endocrine-disrupting effects at high doses. This thesis investigates the risks associated with IFs and enterolactone (ENL), another notable phytoestrogen, and explores strategies for promoting safe soy consumption.Objectives:1. Assess French exposure to IFs and ENL, and validate tools for accurate estimation.2. Investigate the endocrine effects of IFs and ENL in humans, focusing on systemic lupus erythematosus (SLE) and triple-negative breast cancer.3. Develop techniques to reduce the IFs content of soy-based food products.Methodology:(1) IF and ENL Exposure Assessment:- Food analyses and dietary intake assessment to quantify the French exposure to IFs and lignans.- Development and validation of food questionnaire to evaluate soy and lignans consumption.- Measurements of IFs and ENL in biological fluids (blood, urine) and hair.(2) Endocrine effects of IFs and ENL:- Case-control study on SLE, comparing IFs and ENL exposure in patients and in healthy controls.- In vitro studies on triple-negative breast cancer cells, analyzing the effect of IFs on cell proliferation and their interactions with the GPER, a membrane estrogen receptor.(3) Reduction of IF levels:- Development of (pre)industrial rinsing processes to decrease IFs content in soybeans.- Investigation of traditional Asian recipes and domestic water rinsing techniques for reducing IFs in soy-based foods.Results:(1) IFs and Lignans exposure:- French exposure to IFs is significant, even for non-soy consumers, due to “hidden soy” in ultra-processed foods.- The developed food questionnaires are validated, and a method for IFs and ENL analysis in hair is presented.(2) Endocrine effects of IFs and ENL:- Preliminary findings from the SLE cohort suggest a potential association between ENL and a healthier status. However, the limited sample size necessitates further investigation to definitively exclude an impact of IFs.- IFs and their circulating conjugates might promote triple-negative breast cancer cells proliferation through the GPER.(3) Reducing IF levels:- Industrial rinsing processes can effectively reduce IFs content in soybean by 50%.- Traditional Asian preparation methods and domestic rinsing significantly decrease IFs in soy-based products.Discussion:Soy consumption warrants specific attention due to the endocrine effects of IFs. Further research is crucial to gain a more comprehensive understanding of these effects and formulate recommendations for safe soy consumption.Conclusion:While soy consumption holds nutritional value and boasts a long tradition in Asia, its high isoflavone content raises questions about its potential impact on human health. This thesis contributes preliminary insights into French exposure to IFs, their possible effects on SLE and triple-negative breast cancer, and proposes solutions for mitigating IFs levels in soy-based foods
Boutry, Nathalie. "Apport de l'imagerie dans la caractérisation des affections synoviales". Lille 2, 2004. http://www.theses.fr/2004LIL2S029.
Texto completoThrough recent technological advances, magnetic resonance (MR) imaging and high-frequency ultrasound (US) have provided new methods for diagnosing early rheumatoid arthritis (RA) and therefore, managing patients. The purpose of my work was threefold: 1. To precise the MR features of metatarsophalangeal (MTP) joints in early RA and to compare MR imaging involvement of MTP joints with that of the hands. Involvement of MTP joints is a classical feature of early RA and can precede involvement of the hands. Until now, there was no relevant reports in the literature about the MR imaging characteristics of the forefeet in early RA. 2. To assess the diagnostic value of MR imaging in patients who present with inflammatory polyarthralgia of the hands. In such a case, diagnosing early RA can be difficult. Moreover, other diagnoses such as systemic lupus erythematosus and primary Sjogren syndrome have to be considered by the clinician. The diagnostic value of MR imaging in differentiating patients with true RA from those with systemic lupus erythematosus and primary Sjogren syndrome was not yet evaluated. 3. To define normal criteria regarding metacacarpophalangeal (MCP) joint anatomy with high-resolution US. Recent technological advances in the field of US have been responsible for great interest. However, the normal anatomy of MCP joints remained unclear. My results are the following: 1. Except the fact that intermetatarsal and submetatarsal bursitis is a common MR finding (63% of cases), MR imaging involvement of MTP joints in patients with early RA is similar to that of hand joints. There is no differences between MCP and MTP joints in terms of bone erosions. When MR evaluation of the hands does not help identify early RA, further evaluation of the MTP joints may be helpful. 2. Except for subchondral edema (which is more frequent within the MCP joints in patients with early RA), it may be impossible to differentiate patients with early RA from those with systemic lupus erythematosus and primary Sjogren syndrome. 3. High-frequency US provides detailed and reliable assessment of MCP joints. Quantitative data related to synovial structures are also reported. These works enabled us to better precise MR and US features of early RA. They show our collaboration with the Rheumatology and Internal Medicine departments as well as the Anatomic department of our Medicine Faculty. We also collaborate with the Heudiasyc laboratory (UMR CNRS 6599) in order to develop a semiautomatic recognition of RA lesions (ie, synovitis and bone erosions)
Dueymes, Maryvonne. "Approche expérimentale du traitement des glomérulonéphrites lupiques par immunomodulation de la stimulation polyclonale". Lyon 1, 1989. http://www.theses.fr/1989LYO1H082.
Texto completoSawaf, Matthieu. "Le récepteur co-inhibiteur BTLA au cours du lupus érythémateux disséminé (LED) : aspects fondamentaux et implications thérapeutiques". Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ016.
Texto completoSystemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by lesions in several organs such as kidneys, lungs and skin for instance. In this pathology, an excessive activation of the immune system leads to the production of autoantibodies targeting mainly nuclear antigens. B cell differentiation into antibody-secreting cells requires a close collaboration between T and B cells. This cross-talk is regulated by various cellular and molecular factors in order to mount an efficient humoral response in case of infection, but also to prevent autoimmune disease development. The aim of my thesis was to study two regulating factors of the B cell response, one promoting the B cell differentiation into plasma cells, i.e the follicular helper T cells (TFH) and the other one inhibiting lymphocyte activation, i.e a co-inhibitory receptor called BTLA (« B and T Lymphocyte Attenuator ») in human SLE. In this study, we first improved our knowledge concerning human circulating TFH cells, by describing among the CXCR3-CCR6- TFH cell subset, a population with suppressive capacities. Moreover, we suggested that the decreased frequency of TFH1 in lupus patients’ blood could be explained by the migration of these cells into inflamed tissues. We also highlighted a BTLA functional deficiency in lupus CD4+ T cells. This deficiency, which can be restored by normalizing the lipid metabolism, seems to be associated to disease severity. Furthermore, we described an altered expression of BTLA in lupus B cells and regulatory T cells. Altogether, our data show promising results and suggest new potential therapeutic strategies for lupus treatment
Thébault, Sandrine. "Application de l'analyse protéomique ciblée à l'étude de la réponse autoimmune B au cours du lupus érythémateux disséminé dans le modèle murin (NZW x BXSB)F1". Rouen, 2003. http://www.theses.fr/2003ROUES008.
Texto completoAutoantibodies are produced during systemic lupus erythematosus, an autoimmune disease developed by humans and certain strains of mice. To characterize SLE-related autoantibodies may be crucial to precise the immunogenic stimulus(i) of autoantibody-secreting B lymphocytes. Here with, we showed that two-dimensional electrophoresis combined with mass spectrometry allowed to identify cell proteins recognized by lupus-autoantibodies produced by (NZW X BXSB)F1 mice. These results show that targeted proteomic analysis constitutes a global and sensitive technique to characterize the B immune response and may constitute a new approach to further characterize the immunogenic cellular components involved in the breakage of B-cell tolerance observed in lupus
Moncan, Matthieu. "Pathophysiologie des défauts génétiques du Lupus Erythémateux disséminé pédiatrique : implications du stress du réticulum endoplasmique et de la voie PI3K dans le développement de l’auto-immunité". Thesis, Sorbonne Paris Cité, 2019. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2329&f=17112.
Texto completoOur laboratory discovered in a familial case of lupus an heterozygous mutation or the ERN1 gene coding for the IRE1a protein : the major inducer of the Unfolded Protein Response (UPR). The UPR is a transcriptional program which can restore the function of the endoplasmic reticulum (ER) when it is overloaded with unfolded proteins, a process also called ER stress. The ER stress will induce the UPR by the activation of IRE1a, activating a pro-survival response to return to homeostasis in case of a acute stress or a pro-apoptotic response in case of a chronic stress. By expression the wild type and mutated human version of the protein in the yeast at the homozygous state, we showed that the mutation induces a complete RNAse and a partial kinase loss of function. With a cellular system overexpressiong IRE1a in a HEK293 cell line, we confirmed that the mutated protein can be expressed in human cells despite a strong impact of the mutation on the protein, as showed by our in silico analysis. These results have oriented us towards a dominant negative mutation model as IRE1a works as a dimere or an oligomere. Molecular analysis of the UPR on B lymphocytes immortalized by the Epstein-Barr virus (B-EBV) coming from our patient of interest showed a splicing delay in XBP1, the main target of IRE1a RNAse activity, as we could see it with a diminished XBP1 splice form expression (XBP1s) and an increased unspliced form expression (XBP1u). The XBP1s/XBP1u ratio confirms this temporal dysregulation of the IRE1a-XBP1 pathway which shows increasing activity until 48h in the patient, while the controls already returned to homeostasis. This dysregulation didn't modify the expression of XBP1 transcriptional targets : EDEM1, DNAJB9, DNAJC3. However, the expression of IL6 was greatly increase both at basal state and after tunicamycin treatment. The functional analysis demonstrated a resistance of B-EBV to extrinsic apoptosis in the patient of interest, without any diminution of FAS and TRAIL receptors at the membrane. This resistance could be at the origin of the autoimmune phenotype observable on the family members carrying the mutation. A Western Blot analysis showed a diminished expression of Caspase-3 compared to a control. As Caspase-3 is a target of the RIDD (Regulated IRE1a-dependant decay of mRNA), a mRNA degradation activity linked to the RNAse activity of IRE1a, our hypothesis is that the longer activation of IRE1a will induce a dysregulation of apoptosis induction in the UPR, as IRE1a needs to be desactivated to induce cell death. The IRE1a-XBP1 pathway also presents direct links with the PI3K/Akt pathway : first through the association of XBP1 and p85a/b to increase XBP1 nuclear translocation, second through the inhibition of IRE1a induced by the reactivation of the PI3K/Akt pathway after induction of ER stress. Moreover, two families presenting lupus cases or a clinical table close to our ERN1 patients are also carriers of PIK3R1 and PIK3R2 mutations, coding for p85a and p85b, two proteins essential for the signalisation of the PI3K/Akt pathway. Since this pathway is important for proliferation and cell survival and the fact that our B-EBV ERN1 KO cell line shows a strongly decreased phosphorylation of AKT, we suspect that defects of this pathway could converge to the IRE1a-XBP1 pathway and induce an autoimmunity with a resistance to extrinsic apoptosis. These data underlined the notion of a link between ER stress and autoimmunity, providing a first insight to this field by the description of these monogenic cases of lupus