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Literatura académica sobre el tema "Organe lymphoïde tertiaire"

Autor: Grafiati

Publicado: 7 de diciembre de 2024

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Artículos de revistas sobre el tema "Organe lymphoïde tertiaire"

Shomer, Nirah H., James G. Fox, Amy E. Juedes y Nancy H. Ruddle. "Helicobacter-Induced Chronic Active Lymphoid Aggregates Have Characteristics of Tertiary Lymphoid Tissue". Infection and Immunity 71, n.º 6 (junio de 2003): 3572–77. http://dx.doi.org/10.1128/iai.71.6.3572-3577.2003.

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ABSTRACT Susceptible strains of mice that are naturally or experimentally infected with murine intestinal helicobacter species develop hepatic inflammatory lesions that have previously been described as chronic active hepatitis. The inflammatory infiltrates in some models of chronic autoimmunity or inflammation resemble tertiary lymphoid organs hypothesized to arise by a process termed lymphoid organ neogenesis. To determine whether hepatic inflammation caused by infection with helicobacter could give rise to tertiary lymphoid organs, we used fluorescence-activated cell sorting, immunohistochemistry, and in situ hybridization techniques to identify specific components characteristic of lymphoid organs in liver tissue sections and liver cell suspensions from helicobacter-infected mice. Small venules (high endothelial venules [HEVs]) in inflammatory lesions in Helicobacter species-infected livers were positive for peripheral node addressin. Mucosal addressin cell adhesion molecule also stained HEVs and cells with a staining pattern consistent with scattered stromal cells. The chemokines SLC (CCL 21) and BLC (CXCL13) were present, as were B220-positive B cells and T cells. The latter included a naïve (CD45lo-CD62Lhi) population. These findings suggest that helicobacter-induced chronic active hepatitis arises through the process of lymphoid organ neogenesis.

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Barone, Francesca, Saba Nayar, Joana Campos, Thomas Cloake, David R. Withers, Kai-Michael Toellner, Yang Zhang et al. "IL-22 regulates lymphoid chemokine production and assembly of tertiary lymphoid organs". Proceedings of the National Academy of Sciences 112, n.º 35 (18 de agosto de 2015): 11024–29. http://dx.doi.org/10.1073/pnas.1503315112.

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The series of events leading to tertiary lymphoid organ (TLO) formation in mucosal organs following tissue damage remain unclear. Using a virus-induced model of autoantibody formation in the salivary glands of adult mice, we demonstrate that IL-22 provides a mechanistic link between mucosal infection, B-cell recruitment, and humoral autoimmunity. IL-22 receptor engagement is necessary and sufficient to promote differential expression of chemokine (C-X-C motif) ligand 12 and chemokine (C-X-C motif) ligand 13 in epithelial and fibroblastic stromal cells that, in turn, is pivotal for B-cell recruitment and organization of the TLOs. Accordingly, genetic and therapeutic blockade of IL-22 impairs and reverses TLO formation and autoantibody production. Our work highlights a critical role for IL-22 in TLO-induced pathology and provides a rationale for the use of IL-22–blocking agents in B-cell–mediated autoimmune conditions.

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Erlich, Emma, Rafael Czepielewski, Shashi Kumar, Rachael Field, Xinya Zhang, Leila Saleh, Farshid Guilak, Jonathan Brestoff, Ali Ellebedy y Gwendalyn J. Randolph. "B cells drive tertiary lymphoid organ formation in ileal inflammation". Journal of Immunology 208, n.º 1_Supplement (1 de mayo de 2022): 113.18. http://dx.doi.org/10.4049/jimmunol.208.supp.113.18.

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Abstract Crohn’s disease [CD] is one of the two most common forms of inflammatory bowel disease, affecting over half a million Americans. Like many other diseases with chronic inflammation, some patients with CD develop tertiary lymphoid organs [TLO] in areas of the gastrointestinal tract with active disease. TLOs are organized clusters of lymphocytes, similar in structure to secondary lymphoid organs, though they develop after birth and their contribution to pathogenesis in CD, or other diseases, is unclear. We, and others, have also found B cell rich lymphoid aggregates in the mesenteric fat of CD patients along dramatically remodeled lymphatic vessels. TNFΔARE/+ is a murine model of ileal inflammation that recapitulates several key features of ileal CD, including development of mesenteric tertiary lymphoid organs. Use of this model revealed that mesenteric TLOs block cellular and molecular export from the gut, leading us to wonder if mechanisms that interfere with their development might reduce ileitis. TNFΔARE/+ mice that lack B cells revealed that B cells are required for tertiary lymphoid organ formation in this model. Without these TLOs, lymphatic outflow from the intestine was restored. Nonetheless, histological and flow cytometric approaches reveal no difference in local inflammation in the ileum. However, systemic inflammation, as assessed by metabolic cages and changes in body weight over time, increased. This suggests that TLOs may act to trap inflammatory signals locally, preventing systemic dissemination of inflammatory cells or mediators. Work supported by NIH grants DP1-DK109668-04 and T32-DK077653-27 and the Kenneth Rainin Foundation

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Ruddle, Nancy H. "Lymphatic vessels and tertiary lymphoid organs". Journal of Clinical Investigation 124, n.º 3 (3 de marzo de 2014): 953–59. http://dx.doi.org/10.1172/jci71611.

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Kirsh, Andrew L., Sharon L. Cushing, Eunice Y. Chen, Stephen M. Schwartz y Jonathan A. Perkins. "Tertiary Lymphoid Organs in Lymphatic Malformations". Lymphatic Research and Biology 9, n.º 2 (junio de 2011): 85–92. http://dx.doi.org/10.1089/lrb.2010.0018.

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Feizi, Neda, Neda Feizi, Gang Zhang, Latha Halesha, Khodor Abou Daya y Martin H. Oberbarnscheidt. "Tertiary Lymphoid Organs promote allograft rejection". Journal of Immunology 212, n.º 1_Supplement (1 de mayo de 2024): 0321_5062. http://dx.doi.org/10.4049/jimmunol.212.supp.0321.5062.

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Abstract Tertiary lymphoid organs (TLOs) are ectopic lymphoid structures that arise in non-lymphoid tissues and are frequently observed in tissue affected by non-resolving chronic inflammation. If TLOs are beneficial or detrimental in transplantation is controversial. We investigate the role of TLO and LTbR in transplantation by manipulating the LTa-LTbR pathway. Using a mouse allo kidney transplantation model, we found that preformed intragraft TLO are sufficient to precipitate rejection in recipients lacking all secondary lymphoid organs (SLO)(LTbRko). In WT recipients with a complete set of SLO, intragraft TLO accelerated rejection (MST=63 vs. 225 d). Donor grafts that cannot form TLO (LTbRko) prolonged allograft survival (MST 24 vs 11 d) in an acute kidney rejection model. Intravital imaging confirmed that T and B cell activation takes place in renal TLO upon migration of naïve T and B cells and prolonged interactions with dendritic cells. T cells produced IFNg and Confetti+/+ B cells clonally expanded within TLO. In summary, intragraft TLO are sufficient for and accelerate allograft rejection. Local immune responses are initiated and maintained in intragraft TLO, while disruption of TLO formation in the allograft leads to prolonged allograft survival. TLO support T and B cell activation as well as local DSA formation. These findings highlight the importance of TLO in local immune responses with implications for cancer, autoimmunity and transplantation.

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Goyal, Girija, Lucas Barck, Yunhao Zhai, Pranav Prabhala, Sudip Paudel, Min Wen Ku, Aditya Patil, Abdul Isaacs y Donald Ingber. "Human implantable tertiary lymphoid organs (TLO) for solid tumor therapy: from organ chips to the clinic?" Journal of Immunology 212, n.º 1_Supplement (1 de mayo de 2024): 0731_7312. http://dx.doi.org/10.4049/jimmunol.212.supp.0731.7312.

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Abstract We previously created an in vitro human TLO model from patient-derived, circulating immune cells using organ-on-a-chip devices and 3D culture in extracellular matrix (ECM). B cells in these TLOs express activation induced cytidine deaminase, which is only expressed in lymphoid tissues and is required for class switching and somatic hypermutation (SHM). When challenged by vaccines, these TLO undergo SHM and produce antigen-specific antibodies and CD8 T cells. To model cancer associated TLOs, we integrated human pancreatic and lung cancer cell lines into these TLO Chips to understand how the immune context of hot and cold tumors differentially impacts TLO formation. The high PDL1/L2 expressing lung cancer cell line that displayed a “hot” phenotype in published murine studies induced high levels of cytokines and stimulated increased TLO formation in the lymphoid Organ Chip. In contrast, the cold, low PDL1/L2 expressing lung and pancreatic cell lines did not induce this cytokine signature or TLO formation. Importantly, TLO assembly correlated with increased B cell activation, anti-tumor CD8 activity, and tumor cell death. When the same mix of immune cells and ECM was injected in humanized mice bearing subcutaneous tumors from the hot lung cancer cell line, new lymphoid tissue containing dense aggregates of T and B cells was induced, showing for the first time that direct injection of synthetic TLOs at the tumor site may offer an alternative form of therapy for solid tumors.

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Lau, Aden, Susan Lester, Sophia Moraitis, Judy Ou, Alkis J. Psaltis, Shaun McColl, Maureen Rischmueller, Peter-John Wormald y Sarah Vreugde. "Tertiary lymphoid organs in recalcitrant chronic rhinosinusitis". Journal of Allergy and Clinical Immunology 139, n.º 4 (abril de 2017): 1371–73. http://dx.doi.org/10.1016/j.jaci.2016.08.052.

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Neyt, Katrijn, Frédéric Perros, Corine H. GeurtsvanKessel, Hamida Hammad y Bart N. Lambrecht. "Tertiary lymphoid organs in infection and autoimmunity". Trends in Immunology 33, n.º 6 (junio de 2012): 297–305. http://dx.doi.org/10.1016/j.it.2012.04.006.

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Shipman, William D., Dragos C. Dasoveanu y Theresa T. Lu. "Tertiary lymphoid organs in systemic autoimmune diseases: pathogenic or protective?" F1000Research 6 (28 de febrero de 2017): 196. http://dx.doi.org/10.12688/f1000research.10595.1.

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Tertiary lymphoid organs are found at sites of chronic inflammation in autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. These organized accumulations of T and B cells resemble secondary lymphoid organs and generate autoreactive effector cells. However, whether they contribute to disease pathogenesis or have protective functions is unclear. Here, we discuss how tertiary lymphoid organs can generate potentially pathogenic cells but may also limit the extent of the response and damage in autoimmune disease.

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Tesis sobre el tema "Organe lymphoïde tertiaire"

Veber, Romain. "Néogenèse lymphoïde au cours du lupus : mécanismes fondamentaux et pistes thérapeutiques". Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ092.

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Le lupus érythémateux disséminé est une maladie auto-immune systémique chronique dont les atteintes sont multiples, l’atteinte rénale constituant la plus sévère. Une conjonction de facteurs génétiques et environnementaux conduit au développement de la maladie qui se traduit par une rupture de tolérance au soi. L’un des signes biologiques majeurs est la production d’auto-anticorps dirigés contre des composants nucléaires qui, en se déposant dans divers tissus dont les reins, génèrent une inflammation chronique conduisant au dysfonctionnement de l’organe. Le dépôt d’autoanticorps s’accompagne d’infiltrats de cellules immunitaires, qui, dans ce type d’inflammation, peuvent se transformer en structures lymphoïdes ectopiques fonctionnelles appelées Organes Lymphoïdes Tertiaires (OLT). Des OLT sont retrouvés dans diverses pathologies et participent à la génération locale de réponses immunitaires bénéfiques (infections/cancers) ou délétères (maladies auto-immunes). Mon projet de thèse a porté sur la mise en évidence d’OLT dans les reins au cours du lupus et sur l’étude des mécanismes permettant leur formation. Nous avons tout d’abord caractérisé les infiltrats inflammatoires présents dans les reins de souris NZB/W, modèle murin spontané de lupus. Ces infiltrats sont hautement organisés et constituent des OLT fonctionnels, potentiellement impliqués dans la néphrite lupique. Nous nous sommes ensuite intéressés aux mécanismes de mise en place de ces OLT et avons identifié les lymphocytes T et le récepteur aux chimiokines CXCR3 comme des éléments clés de ce processus et de la pathologie lupique. Les données obtenues apportent une meilleure compréhension fondamentale de la néogenèse lymphoïde au cours du lupus et ouvrent la voie vers de nouvelles stratégies thérapeutiques permettant de traiter la néphrite lupique
Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease with multiple outcomes, with renal damage being the most severe. A combination of genetic and environmental factors leads to the development of the disease, which results in a break of immune tolerance. One of the major biological signs is the production of autoantibodies to nuclear components that, by depositing in various tissues including the kidneys, generate chronic inflammation leading to organ dysfunction. Deposition of autoantibodies is accompanied by immune cell infiltrates, which in this type of inflammation can be transformed into functional ectopic lymphoid structures called Tertiary Lymphoid Organs (TLO). TLO are found in various diseases and participate in the local generation of beneficial (infections / cancers) or deleterious (autoimmune diseases) immune responses. My thesis project focused on the demonstration of TLO in the kidneys during lupus and on the study of the mechanisms allowing their formation. We first characterized the inflammatory infiltrates present in the kidneys of NZB/W mice, a spontaneous murine model of lupus. These infiltrates are highly organized and constitute functional TLO that are potentially implicated in lupus nephritis. We then investigated the mechanisms of development of these TLO and identified T lymphocytes and the CXCR3 chemokine receptor as key components of this process and lupus pathology. The data obtained provide a better understanding of lymphoid neogenesis during lupus and pave the way for new therapeutic strategies to treat lupus nephritis

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Fouet, Morgane. "Modulation du microenvironnement tumoral et de la réponse immunitaire par des virus oncolytiques modifiés". Electronic Thesis or Diss., Nantes Université, 2024. http://www.theses.fr/2024NANU1008.

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Les virus présentant un tropisme pour les cellules tumorales et une capacité à induire leur lyse, sont appelé des virus oncolytiques. Ils sont utilisés dans le cadre de la virothérapie et permettent de stimuler la réponse immunitaire antitumorale par le recrutement et l’activation de cellules immunitaires innées et adaptatives. Les travaux issus de ma thèse ont permis d'approfondir la compréhension du rôle des lymphocytes Tϒ9δ2 dans le cadre des infections oncolytiques, en mettant notamment en lumière leur activation spécifique par la souche Schwarz du virus de la rougeole. J’ai ensuite développé un virus oncolytique capable de coder pour un anticorps conçu pour activer de manière ciblée les lymphocytes Tϒδ. L’évaluation thérapeutique de ce virus dans un modèle murin a révélé des résultats prometteurs, notamment sur le contrôle de la croissance tumorale. Par ailleurs, j’ai développé une stratégie thérapeutique visant à favoriser la formation d'organes lymphoïdes tertiaires au sein du micro-environnement tumoral. En utilisant un virus oncolytique pour vectoriser des protéines clés de la néo-genèse des organes lymphoïdes tertiaires, j'ai observé que la combinaison de trois virus distincts facilite l’infiltration non seulement des lymphocytes T, mais aussi des lymphocytes B dans le micro-environnement tumoral. Cette approche offre une perspective prometteuse pour améliorer la réponse immunitaire antitumorale et mérite une exploration plus approfondie pour confirmer son potentiel clinique
Viruses exhibiting a tropism for tumor cells and an ability to induce their lysis, are called oncolytic viruses. They are used in the context of virotherapy and make it possible to stimulate the anti-tumor immune response by recruiting and activating innate and adaptive immune cells. The work resulting from my thesis made it possible to deepen the understanding of the role of ϒ9δ2 T cells in the context of oncolytic infections, in particular by highlighting their specific activation by the Schwarz strain of the Measles virus. | then developed an oncolytic virus capable of encoding an antibody designed to specifically activate ϒδ T cells. Therapeutic evaluation of this virus in a mouse model revealed promising results, particularly on the control of tumor growth. Furthermore, | developed a therapeutic strategy aimed at promoting the formation of tertiary lymphoid structures within the tumoral microenvironment. Using an oncolytic virus to vectorize key proteins in tertiary lymphoid structures neogenesis, | observed that the combination of three distinct viruses facilitates the infiltration of not only T cells, but also B cells into the tumoral microenvironment. This approach offers a promising prospect for improving the antitumor immune response and deserves further exploration to confirm its clinical potential

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Motallebzadeh, Reza. "Tertiary lymphoid organogenesis in solid organ transplantation". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608121.

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Nayar, Saba. "Lymphoid like stromal cells in a model of tertiary lymphoid organ formation". Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5245/.

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Tertiary lymphoid organs (TLOs) are a hallmark of many chronic immune-mediated inflammatory diseases. However, till date the series of events leading to stromal cell activation in TLOs and their role in the inflammatory process remain unclear. Using a model of inducible TLO formation in the salivary glands of mice we explored the role of gp38+LTβR+ lymphoid-like stromal cells (LLSc) during TLO development and show that they acquire the capability to produce lymphoid chemokines (CKs)/cytokine and drive lymphocyte compartmentalization. In this thesis, we provide evidence that stromal cell activation is a multi-step process with three distinct phases mediated by three major cytokines (IL-13, IL-22 and LTβ). We demonstrate that during TLO formation, IL-4Rα engagement via IL-13 on quiescent tissue-resident fibroblasts induces the phenotypic acquisition of lymphoid features by LLSc. IL22 then initiates the proliferation and expansion of the LLSc population, required for the expression of lymphoid CKs/cytokines and ANA autoantibody production. Finally, we show that LTβR ligation is necessary for the establishment of a fully mature TLO structure once IL-22 driven LLSc proliferation has occurred. Based on our findings we have identified three different phases of stromal cell activation in TLOs which are all potentially targets of future therapy.

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Le, Coz Carole. "Quelle contribution du centre germinatif et de ses composants moléculaires et cellulaires dans la physiopathologie du lupus ?" Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ077.

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Le lupus érythémateux disséminé est une maladie auto-immune systémique très invalidante dont les atteintes sont multiples, les plus fréquentes étant cutanées, articulaires et rénales. Dans ce type de maladie, le système immunitaire, hyperactif, ne se limite pas à lutter contre des agents extérieurs mais s'attaque à ses propres cellules, entre autres par le biais d'auto-anticorps. Ces anticorps délétères sont produits par des plasmocytes, cellules issus de la différenciation des lymphocytes B. Ce processus se déroule principalement au sein des centres germinatifs (GC) dans les organes lymphoïdes secondaires, et fait intervenir de nombreux acteurs moléculaires et cellulaires. Mon projet de thèse a porté sur l'étude de la contribution du GC et de ses constituants, tels que les cellules auxiliaires folliculaires (Tfh) et l'IL-21, au cours du lupus. Au cours de ce travail, nous avons mis en évidence une altération à la fois quantitative et qualitative des cellules Tfh chez des patients lupiques et dans un modèle murin, altération entre autres responsable de taux anormalement élevés d'IL-21. Nous avons également observé une sensibilité accrue des cellules B de souris lupiques à cette cytokine, dont la cause est une surexpression de molécules clés telles que STAT3, et dont la conséquence est un surcroit de différenciation plasmocytaire. Tous les éléments sont donc présents pour favoriser l'interaction "Tfh-B" et la réaction du GC, et amplifier la réponse autoimmune. Enfin, la découverte de l'existence de GC ectopiques fonctionnels dans les reins de souris lupiques permet d'envisager l'existence de réponses locales au sein même des organes cibles. Les données obtenues, fondamentales, sont prometteuses et laissent entrevoir de nouvelles perspectives de biothérapies, plus ciblées, pour le traitement de la maladie lupique
Systemic lupus erythematosus is a disabling chronic autoimmune disease characterized by B cell hyperactivity leading to the production of autoantibodies, some of which exerting pathogenic effects. Autoantibodies are produced by plasma cells, which originate from the differentiation of B cells through a process that mainly takes place in germinal centers (GC) in secondary lymphoïd organs and involves many molecular and cellular parameters. The aim of my PhD project was to analyze the individual contribution of GC components, such as follicular helper T cells (Tfh) and IL-21, to lupus development. During this work, we have shown both a quantitative and qualitative impairment of Tfh cells in lupus patients and in a mouse model, leading, among other things, to high IL-21 levels. We also observed that B cells from lupus mice display a specific intrinsic sensitivity to this cytokine, due to over-expression of key molecules such as STAT3, which results in increased plasma cell differentiation. Thus, all elements are gathered that favor "Tfh-B" cell interactions and the GC reaction, and therefore the autoimmune response. Finally, the discovery of functional ectopic GC in the kidneys of lupus mice allows envisaging that local responses occur within the target organs and likely participate to kidney injury. The fundamental data we obtained are promising and anticipate new and better targeted biotherapies for lupus treatment

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Browne, Eleanor. "Tertiary lymphoid organ neogenesis in grey matter pathology in multiple sclerosis". Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/30813.

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Chronic meningeal inflammation is suggested to contribute to the progression of secondary progressive multiple sclerosis (SPMS) in part by driving cortical grey matter pathology. The presence of tertiary lymphoid organ-like (TLO) structures in a large proportion of SPMS cases is associated with faster clinical progression and more severe cortical pathology, suggesting that TLO neogenesis and chronic meningeal inflammation contribute to progression. Gene expression of the cytokine lymphotoxin-alpha (LTα), implicated in TLO formation and cytotoxicity, and the lymphoid chemokines CXCL13 and CCL21, was determined in post-mortem SPMS meninges by qPCR. LTα was increased in SPMS, while substantially increased CXCL13 expression was associated with the presence of TLOs in SPMS. As LTα induces CXCL13 during inflammation, we investigated the hypothesis that LTα drives TLO formation and exacerbates cortical pathology in SPMS, using an animal model of cortical demyelination driven by meningeal inflammation. Subclinical experimental autoimmune encephalomyelitis was induced in female dark agouti rats by immunisation with 5-10μg of recombinant mouse myelin oligodendrocyte glycoprotein (rmMOG) in incomplete Freund's adjuvant. Injection of LTα and the cytokine interferon-γ into the subarachnoid space 21 days post-immunisation induced substantial meningeal infiltration with B cell-rich areas, T cells, macrophages and channel formation reminiscent of early TLOs, accompanied by microglial activation, extensive demyelination, and remyelination within 21 days. To study chronic meningeal cytokine expression we injected a VSV-G pseudotyped lentiviral vector (LV) expressing green fluorescent protein (GFP) or human LTα (LVLTα) into the subarachnoid space. Meningeal GFP expression was induced up to 90 days post-injection. Human LTα expression was detected in rat brain and CSF, with widespread microglial activation and meningeal infiltrates of macrophages, B and T cells resembling TLOs, in naïve and rmMOG-immunised rats at 90 days post-LVLTα, while extensive demyelination was present only in rmMOG-immunised rats. This suggests that chronic meningeal LTα expression is sufficient for widespread microglial activation, but demyelination requires an anti-myelin response in this model. These findings support the hypothesis that chronic meningeal inflammation drives cortical pathology, and LTα/TLO neogenesis may represent a novel therapeutic target for SPMS.

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Dias, De Campos Joana. "The pleomorphic role of stromal cells in the formation and maintenance of tertiary lymphoid organs". Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6994/.

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A large body of evidence supports the role of activated stromal cells in the persistence of inflammation. The switch from resting to pathogenic stroma appears to be associated with the development of tertiary lymphoid organs (TLOs) within sites of chronic inflammation. However little is known about the immunological function of the stromal component. We utilised a murine model of inducible TLO formation in inflamed salivary glands to investigate the role of activated stromal cells characterised by the expression of gp38 and FAP during TLO development. We demonstrated that during inflammation, stroma-derived ICOSL engages ICOS on T cells, necessary for the release of lymphotoxin α and consequent TLO formation. Whilst dissecting the role of stromal cells in this context, we demonstrate that gp38 expression is required for the upregulation of adhesion molecules involved in cell clustering. Depletion of gp38+FAP+ stromal cells led to a significant reduction in lymphoid chemokine production, a decreased number of infiltrating lymphocytes and severely compromised TLO formation. Collectively, we provide evidence that activated stromal cells express FAP, provide co-stimulatory signals, and are necessary for the establishment of viral-induced TLOs, highlighting a potential novel therapeutic target in TLO-associated autoimmune diseases.

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Winter, Susann. "Funktionale Bedeutung der homöostatischen Chemokinrezeptoren CCR7 und CXCR5 im Verlauf von mukosalen Immunantworten". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16328.

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Die kontinuierliche Rezirkulation von Immunzellen durch periphere und sekundäre lymphatische Organe (SLOs) ist Bestandteil der Immunüberwachung und wichtig für die Aufrechterhaltung und Funktionsbereitschaft des Immunsystems. Der homöostatische Chemokinrezeptor CCR7 vermittelt dabei nicht nur die Rezirkulation von Lymphozyten durch SLOs, sondern scheint auch an der homöostatischen Rezirkulation von Lymphozyten durch nicht-lymphoide periphere Gewebe beteiligt zu sein. Im Rahmen dieser Arbeit wurde mithilfe von CCR7-defizienten Mäusen die funktionale Bedeutung von CCR7 für die homöostatische Rezirkulation von Lymphozyten durch das Peritoneum untersucht und nachgewiesen, dass CCR7 der dominante Chemokinrezeptor ist, der unter physiologischen Bedingungen die Transitzeit von Lymphozyten durch das Peritoneum festlegt. Die gestörte Rezirkulation von Lymphozyten begünstigte außerdem die Entstehung von tertiären lymphoiden Organen (TLOs) in der Magenschleimhaut von CCR7-defizienten Mäusen. Untersuchungen zur zellulären und molekularen Grundlage dieser und weiterer pathomorphologischer Veränderungen in der Magenschleimhaut von CCR7-defizienten Mäusen verdeutlichten die Funktion von CCR7 für die Etablierung von zentraler und peripherer Toleranz gegenüber gastrischen Antigenen. Fehlt CCR7, dann entwickelten Mäuse eine spontane Autoimmungastritis, welche durch gastritogene CD4+ T-Zellen verursacht wurde, deren Aktivierung auch unabhängig von Lymphknoten und TLOs erfolgte. Die Entstehung von TLOs wird auch bei einer durch Helicobacter pylori ausgelösten chronischen Gastritis beobachtet. Die Expression des homöostatischen Chemokinrezeptors CXCR5 und seines Liganden CXCL13 ist mit der Entwicklung dieser TLOs korreliert worden. Unter Verwendung eines Mausmodells für H. pylori-induzierte chronische Gastritis konnte gezeigt werden, dass CXCR5 die Ausbildung von TLOs vermittelt und eine Rolle für die Induktion von H. pylori-spezifischen T-Zell- sowie humoralen Immunantworten spielt.
Homeostatic recirculation of immune cells through peripheral and secondary lympoid organs (SLOs) is required for immune surveillance and the maintenance and functionality of the immune system. The homeostatic chemokine receptor CCR7 controls not only lymphoid cell trafficking to and within SLOs, but also seems to be involved in the homeostatic recirculation of lymphocytes through non-lymphoid peripheral tissues. Within the scope of this work we investigated the functional relevance of CCR7 for the homeostatic recirculation of lymphocytes through the peritoneal cavity and could show, that CCR7 is the dominant chemokine receptor which defines the transit time of lymphocytes in the peritoneal cavity under physiological conditions. Impaired recirculation of lymphocytes also promoted the development of tertiary lymphoid organs (TLOs) in the gastric mucosa of CCR7-deficient mice. Analysis of the cellular and molecular mechanisms underlying these and other pathomorphological alterations in the gastric mucosa of CCR7-deficient mice provided further evidence regarding the function of CCR7 for the establishment of central and peripheral tolerance towards gastric antigens. Mice that lack CCR7 spontaneously developed autoimmune gastritis, which was caused by gastritogenic CD4+ T-cells. Such autoreactive T cell responses were also initiated in the absence of lymph nodes and TLOs in CCR7/LT-alpha double-deficient mice. Development of TLOs is also observed during chronic gastritis induced by Helicobacter pylori. The expression of the homeostatic chemokine receptor CXCR5 and its ligand CXCL13 has been correlated with the development of these TLOs. Using a mouse model for H. pylori-induced chronic gastritis, we could show that CXCR5 is responsible for the development of TLOs and also plays a role for the induction of H. pylori-specific T and B cell responses.

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Hörnblad, Andreas. "Imaging the pancreas : new aspects on lobular development and adult constitution". Doctoral thesis, Umeå universitet, Umeå centrum för molekylär medicin (UCMM), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-50601.

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The mouse pancreas is a mixed exocrine and endocrine glandconsisting of three lobular compartments: the splenic, duodenal and gastric lobes. During embryogenesis, the pancreas forms from two progenitor populations located on the dorsal and ventral side of the primitive gut tube. These anlagen are brought in close proximity as the gut elongates and rotates, and fuse to form a single organ. The splenic and duodenal lobes develop from the dorsal and ventral anlagen, respectively. In the adult pancreas, exocrine tissue secretes digestive enzymes intothe gut lumen to support nutrient uptake. The endocrine Islets of Langerhans are scattered throughout the exocrine tissue and aid in regulation of energy homeostasis through the secretion of hormones. One of the key players in energy homeostasis is the pancreatic ß-cell, which is the most abundant cell type of the islets. The β-cells regulates blood glucose levels through the action of insulin. Conditions where this regulation does not function properly are gathered under the common name of Diabetes mellitus. Type 1 diabetes (T1D) is characterized by insulin deficiency due to autoimmune destruction of the ß-cells. Using recently developed protocols for optical projection tomography (OPT) whole-organ imaging, we have revealed new spatial and quantitative aspects on ß-cell mass dynamics and immune infiltration during the course of T1D development in the non-obese diabetic (NOD) mouse model. We show that although immune infiltration appears to occur asynchronously throughout the organ, smaller islets, mainly located in the periphery of the organ, preferentially loose their ß-cells during early stages of disease progression. Larger islets appear more resistant to the autoimmune attack and our data indicate the existence of a compensatory proliferative capacity within these islets. We also report the appearance of structures resembling tertiary lymphoid organs (TLOs) in association with the remaining islets during later phases of T1D progression. OPT has already proven to be a useful tool for assessments of ß-cellmass in the adult mouse pancreas. However, as with other techniques, previous protocols have relied on a tedious degree of manual postivacquisition editing. To further refine OPT-based assessment of pancreatic ß-cell mass distribution in the murine pancreas, we implemented a computational statistical approach, Contrast-Limited Adaptive Histogram Normalisation (CLAHE), to the OPT projection data of pancreata from C57Bl/6 mice. This methodology provided increased islet detection sensitivity, improved islet morphology and diminished subjectivity in thresholding for reconstruction and quantification. Using this approach, we could report a substantially higher number of islets than previously described for this strain and provide evidence of significant differences in islet mass distribution between the pancreatic lobes. The gastric lobe stood out in particular and contained a 75% higher islet density as compared to the splenic lobe. Although the development of the early pancreatic buds has been relatively well studied, later morphogenetic events are less clear and information regarding the formation of the gastric lobe has largely been missing. Using OPT we have generated a quantitative three-dimensional road map of pancreatic morphogenesis in the mouse. We show that the gastric lobe forms as a perpendicular outgrowth fromthe stem of the dorsal pancreas at around embryonic day (e) 13.5, which grows into a mesenchymal domain overlaying the pyloric sphincter and proximal part of the glandular stomach. By analyzing mutant mice with aberrant spleen development, we further demonstrate that proper formation of the gastric lobe is dependent on the initial formation of the closely positioned spleen, indicating a close interplay between pancreatic and splenic mesenchyme during development. Additionally, we show that the expression profile of markers for pancreatic multipotent progenitors within the pancreas is heterogenous with regards to lobular origin. Altogether, our studies regarding the morphogenesis and adult constitution of the mouse pancreas recognize lobular heterogeneities that add important information for future interpretations of this organ.

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Libros sobre el tema "Organe lymphoïde tertiaire"

Yin, Changjun, Andreas J. R. Habenicht, Sarajo Mohanta y Pasquale Maffia, eds. Tertiary Lymphoid Organs (TLOs): Powerhouses of Disease Immunity. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-180-7.

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Capítulos de libros sobre el tema "Organe lymphoïde tertiaire"

Kobayashi, Yuka, Koichi Kato, Makoto Nakamura y Takeshi Watanabe. "Synthesis of Functional Tertiary Lymphoid Organs". En Synthetic Immunology, 151–69. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56027-2_7.

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Rivellese, Felice, Elena Pontarini y Costantino Pitzalis. "Tertiary Lymphoid Organs in Rheumatoid Arthritis". En Current Topics in Microbiology and Immunology, 119–41. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/82_2020_216.

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Actas de conferencias sobre el tema "Organe lymphoïde tertiaire"

Touzani, Fahd y Agnieszka Pozdzik. "O21 Analysis of B-cell infiltrates and tertiary lymphoid organ in lupus nephritis". En 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.32.

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Conlon, T. M., G. John-Schuster, M. Lehmann, R. Costa, G. Burgstaller, S. E. Verleden, O. Eickelberg, M. Koenigshoff, M. Heikenwalder y Yildirim. "Therapeutic Targeting of B Cell Mediated Tertiary Lymphoid Organs (TLO) Reverts Chronic Obstructive Pulmonary Disease". En American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7674.

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Lehmann, J., M. Thelen, S. Schran, E. Preugszat, K. Wennhold, M. Garcia-Marquez, P. Lohneis et al. "P02.03 Organization, function and gene expression of tertiary lymphoid structures in pancreatic cancer resembles lymphoid follicles in secondary lymphoid organs and their abundance is related to superior survival". En iTOC9 – 9th Immunotherapy of Cancer Conference, September 22–24, 2022 – Munich, Germany. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-itoc9.22.

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Wennhold, K., J. Lehmann, M. Thelen, C. Kreer, M. Garcia-Marquez, P. Lohneis, S. Boeck et al. "03.03 Tertiary lymphoid structures in pancreatic cancer resemble lymphoid follicles in secondary lymphoid organs as sites for initiation and maintenance of anti-tumor T- and B-cell responses". En iTOC10 - 10th Immunotherapy of Cancer Conference, March 21 – 23, 2024 – Munich, Germany. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/jitc-2024-itoc10.1.

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Liu, Xinning, Yun Qiu, Ren Mao y Ziyin Ye. "IDDF2022-ABS-0268 Subserosal tertiary lymphoid organs is a risk factor for postoperative recurrence in Crohn’s disease". En Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 2–4 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-iddf.248.

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Hiraoka, Nobuyoshi. "Abstract B21: Tertiary lymphoid organs within pancreatic ductal carcinoma tissue are a favorable prognosticator, being strongly associated with blood vessels not infiltrated by cancer cells". En Abstracts: AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; March 5-8, 2015; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.tumang15-b21.

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