Academic literature on the topic 'Antigène delta'
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Journal articles on the topic "Antigène delta"
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Djebbi, A., W. K. Rebai, O. Bahri, N. Hogga, A. Sadraoui, and H. Triki. "Marqueurs sérologiques, ARN viral et génotype du virus de l’hépatite delta chez des patients tunisiens antigène HBs positifs." Pathologie Biologie 57, no. 7-8 (November 2009): 518–23. http://dx.doi.org/10.1016/j.patbio.2008.09.010.
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Cornillez-Ty, Cromwell T., and David W. Lazinski. "Determination of the Multimerization State of the Hepatitis Delta Virus Antigens In Vivo." Journal of Virology 77, no. 19 (October 1, 2003): 10314–26. http://dx.doi.org/10.1128/jvi.77.19.10314-10326.2003.
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ABSTRACT Hepatitis delta virus expresses two essential proteins, the small and large delta antigens, and both are required for viral propagation. Proper function of each protein depends on the presence of a common amino-terminal multimerization domain. A crystal structure, solved using a peptide fragment that contained residues 12 to 60, depicts the formation of an octameric ring composed of antiparallel coiled-coil dimers. Because this crystal structure was solved for only a fragment of the delta antigens, it is unknown whether octamers actually form in vivo at physiological protein concentrations and in the context of either intact delta antigen. To test the relevance of the octameric structure, we developed a new method to probe coiled-coil structures in vivo. We generated a panel of mutants containing cysteine substitutions at strategic locations within the predicted monomer-monomer interface and the dimer-dimer interface. Since the small delta antigen contains no cysteine residues, treatment of cell extracts with a mild oxidizing reagent was expected to induce disulfide bond formation only when the appropriate pairs of cysteine substitution mutants were coexpressed. We indeed found that, in vivo, both the small and large delta antigens assembled as antiparallel coiled-coil dimers. Likewise, we found that both proteins could assume an octameric quaternary structure in vivo. Finally, during the course of these experiments, we found that unprenylated large delta antigen molecules could be disulfide cross-linked via the sole cysteine residue located within the carboxy terminus. Therefore, in vivo, the C terminus likely provides an additional site of protein-protein interaction for the large delta antigen.
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Uyemura, K., R. J. Deans, H. Band, J. Ohmen, G. Panchamoorthy, C. T. Morita, T. H. Rea, and R. L. Modlin. "Evidence for clonal selection of gamma/delta T cells in response to a human pathogen." Journal of Experimental Medicine 174, no. 3 (September 1, 1991): 683–92. http://dx.doi.org/10.1084/jem.174.3.683.
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T cells bearing gamma/delta antigen receptors comprise a resident population of intraepithelial lymphocytes in organs such as skin, gut, and lungs, where they are strategically located to contribute to the initial defense against infection. An important unsolved question about antigen-driven gamma/delta T cell responses regards the breadth of their T cell receptor (TCR) repertoire, since many specific epithelial compartments in mice display limited diversity. We have examined the diversity of TCR delta gene expression among human gamma/delta T cells from skin lesions induced by intradermal challenge with Mycobacterium leprae. We show that the vast majority of gamma/delta cells from M. leprae lesions use either V delta 1-J delta 1 or V delta 2-J delta 1 gene rearrangements and, within a given region of the lesion, display limited junctional diversity. This contrasts markedly with the extensive diversity of gamma/delta T cells from peripheral blood of these same individuals, as well as skin from normal donors. These results indicate that the gamma/delta response to M. leprae involves the selection of a limited number of clones from among a diverse repertoire, probably in response to specific mycobacterial and/or host antigens.
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Wu, M., L. van Kaer, S. Itohara, and S. Tonegawa. "Highly restricted expression of the thymus leukemia antigens on intestinal epithelial cells." Journal of Experimental Medicine 174, no. 1 (July 1, 1991): 213–18. http://dx.doi.org/10.1084/jem.174.1.213.
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The TL region of the major histocompatibility complex of the mouse contains dozens of tandemly arranged class I genes, including those encoding the thymus leukemia (TL) antigens. TL antigens have been thought to be expressed only on the surface of some T lineage cells, namely immature thymocytes of some mouse strains (TL+ strains), some leukemia cells, and activated T cells. While the function of TL antigens is unknown, recent studies have implicated the products of at least some TL region class I genes as molecules that present antigens to gamma/delta T cells. Since some gamma/delta T cells are known to be specifically associated with certain epithelial tissues, we have investigated the expression of some TL region class I genes in a variety of epithelium-containing tissues. Our results show that the TL antigen gene of C57BL/6 mice, T3b, and the TL antigen genes of BALB/c mice, T3d (previously T3c) and T18d (previously T13c), are highly expressed in the epithelium of the small intestine. In the case of T3b, we further show, using a T3 product-specific antibody, that its product is expressed on the surface of the columnar epithelial cells. In addition, we demonstrated that two other TL region class I genes of C57BL/6 origin, T9b and T21b, are also expressed nearly exclusively in intestinal epithelial cells. These results are consistent with the hypothesis that the products of these TL region class I genes are recognized by gamma/delta T cell receptors of intestinal intraepithelial lymphocytes, a subset of gamma/delta T cells that is localized in the intestinal epithelium and has a restricted V gamma repertoire. Finally, our study indicates that the relative levels of expression of the two homologous TL antigen genes, T3d and T18d, differ widely between the thymus and the intestine.
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Bluestone, J. A., R. Q. Cron, M. Cotterman, B. A. Houlden, and L. A. Matis. "Structure and specificity of T cell receptor gamma/delta on major histocompatibility complex antigen-specific CD3+, CD4-, CD8- T lymphocytes." Journal of Experimental Medicine 168, no. 5 (November 1, 1988): 1899–916. http://dx.doi.org/10.1084/jem.168.5.1899.
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Analyses of TCR-bearing murine and human T cells have defined a unique subpopulation of T cells that express the TCR-gamma/delta proteins. The specificity of TCR-gamma/delta T cells and their role in the immune response have not yet been elucidated. Here we examine alloreactive TCR-gamma/delta T cell lines and clones that recognize MHC-encoded antigens. A BALB/c nu/nu (H-2d)-derived H-2k specific T cell line and derived clones were both cytolytic and released lymphokines after recognition of a non-classical H-2 antigen encoded in the TL region of the MHC. These cells expressed the V gamma 2/C gamma 1 protein in association with a TCR-delta gene product encoded by a Va gene segment rearranged to two D delta and one J delta variable elements. A second MHC-specific B10 nu/nu (H-2b) TCR-gamma/delta T cell line appeared to recognize a classical H-2D-encoded MHC molecule and expressed a distinct V gamma/C gamma 4-encoded protein. These data suggest that many TCR-gamma/delta-expressing T cells may recognize MHC-linked antigens encoded within distinct subregions of the MHC. The role of MHC-specific TCR-gamma/delta cells in immune responses and their immunological significance are discussed.
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Teitell, M., M. F. Mescher, C. A. Olson, D. R. Littman, and M. Kronenberg. "The thymus leukemia antigen binds human and mouse CD8." Journal of Experimental Medicine 174, no. 5 (November 1, 1991): 1131–38. http://dx.doi.org/10.1084/jem.174.5.1131.
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The thymus leukemia antigen (TLA) is a class Ib, or 'nonclassical' class I molecule, one of several encoded within the Tla locus of the mouse major histocompatibility complex (MHC). It structurally resembles the H-2K, D, and L class I transplantation antigens, which present processed peptides to cytotoxic T lymphocytes (CTLs). Although their function(s) are unknown, there has been recent speculation concerning the possibility that class Ib molecules may present antigens to T cells that express gamma delta T cell antigen receptors (TCRs). In this report, using both a cell-cell adhesion assay and adhesion of T lymphocyte clones to purified plate-bound TLA, we provide evidence that TLA can bind to both human and mouse CD8. We also show that a chimeric class I molecule containing the peptide antigen binding site of Ld and the alpha 3 domain, transmembrane, and cytoplasmic segments of TLA, can support a CD8-dependent immune response by CTLs. These results demonstrate for the first time binding of a class Ib molecule to CD8 with a functional outcome, as is observed for the class I transplantation antigens. The capacity to interact with CD8 has been conserved despite the extensive sequence divergence of TLA in the peptide antigen binding site, suggesting this interaction is highly significant. TLA is expressed by epithelial cells in the mouse small intestine. As these epithelial cells are in close contact with intestinal intraepithelial lymphocytes that are nearly all CD8+, and many of which express the gamma delta TCR, the data are consistent with the hypothesis that TLA is involved in antigen presentation, perhaps to gamma delta-positive lymphocytes in this site.
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Jensen, AW, M. Hokland, H. Jorgensen, J. Justesen, J. Ellegaard, and P. Hokland. "Solitary expression of CD7 among T-cell antigens in acute myeloid leukemia: identification of a group of patients with similar T-cell receptor beta and delta rearrangements and course of disease suggestive of poor prognosis." Blood 78, no. 5 (September 1, 1991): 1292–300. http://dx.doi.org/10.1182/blood.v78.5.1292.1292.
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Abstract In a series of 100 acute myeloid leukemia (AML) patients defined by cytochemistry and immunophenotyping, 20 expressed T-lymphocyte associated antigens on the surface of their blasts. While 15 expressed two or more T-cell antigens, five were found to express only CD7. All patients belonged to the French-American-British type M4, and four were under the age of 40. Despite intensive chemotherapy, four never obtained a complete remission and the fifth died of relapse after an allogenic bone marrow transplantation. While 12 randomly selected T- cell antigen negative AML patients showed only few rearrangements in Ig- or T-cell receptor (TCR) genes, such genetic alterations were demonstrated in four of five patients for the TCR delta gene and in all patients for the TCR beta gene. Interestingly, DNA fragments of similar size were demonstrated in three of five patients for both the beta and delta genes. These data suggest that the solitary presence of CD7 among T-cell antigens in otherwise clearcut AML cases identifies a group of patients with similarities in antigen receptor gene configuration as well as outcome.
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Jensen, AW, M. Hokland, H. Jorgensen, J. Justesen, J. Ellegaard, and P. Hokland. "Solitary expression of CD7 among T-cell antigens in acute myeloid leukemia: identification of a group of patients with similar T-cell receptor beta and delta rearrangements and course of disease suggestive of poor prognosis." Blood 78, no. 5 (September 1, 1991): 1292–300. http://dx.doi.org/10.1182/blood.v78.5.1292.bloodjournal7851292.
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In a series of 100 acute myeloid leukemia (AML) patients defined by cytochemistry and immunophenotyping, 20 expressed T-lymphocyte associated antigens on the surface of their blasts. While 15 expressed two or more T-cell antigens, five were found to express only CD7. All patients belonged to the French-American-British type M4, and four were under the age of 40. Despite intensive chemotherapy, four never obtained a complete remission and the fifth died of relapse after an allogenic bone marrow transplantation. While 12 randomly selected T- cell antigen negative AML patients showed only few rearrangements in Ig- or T-cell receptor (TCR) genes, such genetic alterations were demonstrated in four of five patients for the TCR delta gene and in all patients for the TCR beta gene. Interestingly, DNA fragments of similar size were demonstrated in three of five patients for both the beta and delta genes. These data suggest that the solitary presence of CD7 among T-cell antigens in otherwise clearcut AML cases identifies a group of patients with similarities in antigen receptor gene configuration as well as outcome.
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van der Harst, D., A. Brand, SA van Luxemburg-Heijs, YM Kooij-Winkelaar, FE Zwaan, and F. Koning. "Selective outgrowth of CD45RO+ V gamma 9+/V delta 2+ T-cell receptor gamma/delta T cells early after bone marrow transplantation." Blood 78, no. 7 (October 1, 1991): 1875–81. http://dx.doi.org/10.1182/blood.v78.7.1875.1875.
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Abstract Before and after bone marrow transplantation (BMT) for hematologic malignancies, peripheral blood mononuclear cells from 10 patients were obtained. The relative and absolute numbers of CD3+ T-cell receptor gamma delta+ (TCR gamma delta+) cells, as defined by the reaction of monoclonal antibodies (MoAbs) directed against CD3 and the TCR gamma delta (anti-TCR gamma delta-1), were determined. Before transplantation, eight of nine patients tested had less than 10% CD3+TCR gamma delta+ cells. Consistent increased numbers of gamma delta cells up to eightfold the pretransplant level can be seen in four of nine patients tested within the first 4 months after BMT. The large majority of early posttransplant gamma delta and alpha beta T cells express the CD45RO antigen, which is usually expressed on “memory” cells only. The V-region usage of the TCR gamma delta+ T cells was analyzed using fresh mononuclear cells and MoAbs against known V gamma and V delta regions. For more detailed analysis, CD3+TCR gamma delta+ cells were sorted and cultured in bulk and cloned. Using fresh cells and bulk cultures, mainly V gamma 9+V delta 1-V delta 2+ cells were found during engraftment. Only after 6 weeks post-BMT, V gamma 9-V delta 1+V delta 2- cells appear. Analysis of the V gamma and V delta usage at the clonal level confirmed the observation that early after BMT only V gamma 9+V delta 2+ cells are present, whereas gamma delta T- cell clones expressing other gamma delta TCR phenotypes can only be detected 4 to 6 weeks post-BMT. The predominance of V gamma 9+ cells during early engraftment could be explained by several mechanisms: (A) sequential rearrangements during T-cell development, leading to an early wave of V gamma 9+ cells, or (B) selective outgrowth of preexisting V gamma 9+V delta 2+CD45RO+ TCR gamma delta cells in the bone marrow graft, possibly as a result of antigen driven expansion due to exposure to environmental antigens.
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van der Harst, D., A. Brand, SA van Luxemburg-Heijs, YM Kooij-Winkelaar, FE Zwaan, and F. Koning. "Selective outgrowth of CD45RO+ V gamma 9+/V delta 2+ T-cell receptor gamma/delta T cells early after bone marrow transplantation." Blood 78, no. 7 (October 1, 1991): 1875–81. http://dx.doi.org/10.1182/blood.v78.7.1875.bloodjournal7871875.
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Before and after bone marrow transplantation (BMT) for hematologic malignancies, peripheral blood mononuclear cells from 10 patients were obtained. The relative and absolute numbers of CD3+ T-cell receptor gamma delta+ (TCR gamma delta+) cells, as defined by the reaction of monoclonal antibodies (MoAbs) directed against CD3 and the TCR gamma delta (anti-TCR gamma delta-1), were determined. Before transplantation, eight of nine patients tested had less than 10% CD3+TCR gamma delta+ cells. Consistent increased numbers of gamma delta cells up to eightfold the pretransplant level can be seen in four of nine patients tested within the first 4 months after BMT. The large majority of early posttransplant gamma delta and alpha beta T cells express the CD45RO antigen, which is usually expressed on “memory” cells only. The V-region usage of the TCR gamma delta+ T cells was analyzed using fresh mononuclear cells and MoAbs against known V gamma and V delta regions. For more detailed analysis, CD3+TCR gamma delta+ cells were sorted and cultured in bulk and cloned. Using fresh cells and bulk cultures, mainly V gamma 9+V delta 1-V delta 2+ cells were found during engraftment. Only after 6 weeks post-BMT, V gamma 9-V delta 1+V delta 2- cells appear. Analysis of the V gamma and V delta usage at the clonal level confirmed the observation that early after BMT only V gamma 9+V delta 2+ cells are present, whereas gamma delta T- cell clones expressing other gamma delta TCR phenotypes can only be detected 4 to 6 weeks post-BMT. The predominance of V gamma 9+ cells during early engraftment could be explained by several mechanisms: (A) sequential rearrangements during T-cell development, leading to an early wave of V gamma 9+ cells, or (B) selective outgrowth of preexisting V gamma 9+V delta 2+CD45RO+ TCR gamma delta cells in the bone marrow graft, possibly as a result of antigen driven expansion due to exposure to environmental antigens.
Dissertations / Theses on the topic "Antigène delta"
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Le, Gal Frédéric. "Diversité génétique du virus de l'hépatite delta (HDV) en Europe et en Afrique : caractérisation et implications en virologie médicale." Paris 13, 2007. http://www.theses.fr/2007PA132013.
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Le virus de l’hépatite delta (HDV), est satellite du virus de l’hépatite B. La variabilité génétique de HDV a conduit à la définition de génotypes viraux, présentant une répartition géographique spécifique. Les travaux antérieurs du laboratoire ont permis l’identification de 7 génotypes distincts. L’activité « Centre National de Référence du Virus de l’Hépatite Delta » de notre laboratoire nous a permis de caractériser 606 isolats provenant de patients suivis en France et d’identifier un 8ème génotype (HDV-8). Environ 78% des patients présentaient le génotype majoritaire et ubiquitaire HDV-1, 0. 1% HDV-2, 16. 3% HDV-5, 1. 2% HDV-6, 3. 6% HDV-7 et 0. 9% à HDV-8. La totalité des patients infectés par les virus de types -5, -6, -7 et -8 était d’origine africaine. Une grande diversité génétique a de plus été mise en évidence au sein du génotype HDV-1, conduisant à l’individualisation de 3 sous-types : HDV-1AB (isolats originaires d’Europe/Asie), HDV-1C1 et 1C2 (Afrique). Une étude menée en collaboration avec l’Université d’Istanbul nous a permis de retrouver cette diversité des virus HDV-1 au sein des souches circulant en Turquie. L’ensemble de nos résultats nous a conduit à émettre l’hypothèse que HDV aurait pour origine l’Afrique d’où il aurait suivi le cours des migrations humaines via le Moyen-Orient. Nous avons de plus mis au point un test permettant la quantification plasmatique de l’ARN HDV quel que soit le génotype. Ce test, utilisé en routine au laboratoire, a été utilisé dans 2 études pilotes dans le cadre de collaborations avec d’une part l’hôpital Beaujon (France) et d’autre part l’hôpital Hippokration (Athènes, Grèce). Nos travaux ont permis de montrer la variabilité génétique de HDV. Celle-ci doit être prise en compte dans l’élaboration des tests diagnostics. Des études multicentriques prospectives permettront d’apprécier son retentissement sur le pouvoir pathogène du virus et la prise en charge thérapeutiqueHepatitis Delta Virus (HDV) is satellite of hepatitis B virus. The genetic variability of HDV has led to the definition of viral genotypes, presenting specific geographic distribution. Previous studies in our laboratory have allowed to identify 7 distinct genotypes. Our laboratory is a national reference centre for HDV. This has allowed us to characterize 606 isolates from patients followed in France, and to identify an 8th genotype (HDV-8). Approximately 78% patients were infected by HDV-1, which is the most common genotype. 0. 1% were infected by HDV-2, 16. 3% by HDV-5, 1. 2% by HDV-6, 3. 6% by HDV-7 and 0. 9% by HDV-8. All patients infected by viruses HDV-5, -6, -7 and -8 were of African origin. An important genetic diversity was evidenced among HDV-1 viruses, leading to the individualisation of 3 subtypes : HDV-1AB (isolates from Europe/Asia), HDV-1C1 and 1C2 (Africa). A collaborative study with the University of Istanbul allowed us to confirm this diversity of HDV-1 viruses among isolates circulating in Turkey. Taken together, our results tend to indicate that HDV might have originated from Africa and have followed the course of human migrations via Middle-East. We have developed a test to quantify HDV RNA in plasma whatever the viral genotype. This test, employed for routine diagnosis in our laboratory, was used in 2 pilot studies within the context of collaborations with Beaujon Hospital (France) and Hippokration Hospital (Athens, Greece). We have evidenced and characterized the genetic variability of HDV. This variability should be taken into account for the elaboration of diagnostic tests. Further multicenter prospective studies should allow to estimate the impact of the genetic variability on the course of the disease and on the treatment
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Davodeau, François. "Étude de la physiologie et du répertoire de reconnaissance des lymphocytes T [gamma delta] humains : contribution à l'étude des mécanismes générateurs de la diversité des récepteurs à l'antigène des lymphocytes T." Nantes, 1994. http://www.theses.fr/1994NANT12VS.
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Baron, Christophe. "Etude du polymorphisme du récepteur à l'antigène des lymphocytes T au cours de la tolérance et durant le rejet aigü d'allogreffes : étude d'un modèle préclinique de transplantation rénalechez des miniporcs homozytes et recombinants au locus du CMH." Dijon, 2002. http://www.theses.fr/2002DIJOMU03.
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Chez des lignées de miniporcs homozygotes au CMH, un traitement court par la ciclosporine (CsA)permet d'induire la tolérance aux allogreffes rénales dont le CMH de classe I est allogénique mais dont la classe II est identique au donneur. Cependant, les reins tolérés sont rapidement infiltrés par des lymphocytes T (LT)du receveur. Dans ce travail, nous avons étudié la distribution clonale des LT à la fois chez des animaux tolérants et rejeteurs (non traités par la CsA). Méthode : Dans un premier temps, les séquences nucléotidiques codant pour les 19 régions Vβ, 12 segmetns Jβ de la chaîne b du récepteur à l'antigène des LT (TCR) ont été obtenus. Le polymorphysme de longueur de la région CDR3 des chaînes b incluant ces régions, a été étudié à la fois chez des animaux tolérants et rejeteurs (non traités par la CsA). Résultats : chez les animaux tolérants, nous avons observé 1) une distribution polyclonale parmi les LT circulants mais oligoclonale parmi les LT infiltrant les reins (dominance clonale) 2)la dominance clonale n'affecte pas toujours les mêmes sous familles Vb entre différents animaux 3)sur un même animal la dominance clonale s'approfondit avec le temps après la greffe et est retrouvée identique dans une seconde greffe tolérée, implantée sans CsA 4)une dominance identique à celle du rein est observée après incubation in vitro des cellules d'un receveur tolérant avec des cellules du donneur. Chez les animaux rejeteurs, nous avons trouvé une dominance clonale conservée entre différents animaux aussi bien dans les LT circulants que dans le sang périphérique avant que la dysfonction rénale ne soit détectable. Conclusion : les présents résultats in vivo et in vitro , associés à ceux d'études antérieures, suggèrent que des LT de distribution oligoclonale jouent un rôle actif dans le processus de tolérance aux greffes rénales (ces cellules sont actuellement en cours de caractérisation phénotypique). Enfin, la précocité de la dominance au sein des LT circulants sur des animaux rejeteurs pourrait servir de base à un futur test non invasif de diagnostic précoce de rejet
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Guillaume, Yves. "Caractérisation fonctionnelle de la molécule CD277 dans les lymhocytres T Vγ9Vδ2." Aix-Marseille 2, 2009. http://www.theses.fr/2009AIX20654.
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Baudhuin, Jérémy. "Régulation de l'activité d'effecteurs cellulaires de la réponse immunitaire innée par interaction des récepteurs inhibiteurs ILT2 et ILT4 avec la molécule HLA-G." Paris 7, 2013. http://www.theses.fr/2013PA077207.
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La subversion ou le dysfonctionnement des processus de tolérance de l'immunité innée peuvent conduire au développement de diverses pathologies. D'une part, en interagissant avec le récepteur inhibiteur ILT2 exprimé à la surface des cellules NK et des lymphocytes T y8, la molécule HLA-G permet aux cellules tumorales l'exprimant d'échapper à l'activité anti-tumorale de ces deux populations. En effet, en perturbant l'organisation de la synapse immunologique, et ce indépendamment des radeaux lipidiques, HLA-G entraîne l'inhibition de l'activité cytotoxique des cellules NK. De plus, elle provoque l'inhibition de la prolifération, de la synthèse d'IFN-y et de la cytotoxicité des lymphocytes T y& D'autre part, l'engagement du récepteur ILT4, autre récepteur connu de HLA-G, à la surface des granulocytes neutrophiles, conduit à une diminution de leur fonction phagocytaire et oxydative induites par le récepteur CD32a. Contenu dans les granules intracytoplasmiques des neutrophiles, ILT4 peut être mobilisé en surface par exocytose en réponse à un stimulus pro-inflammatoire, contribuant ainsi à la régulation de leur activité inflammatoire. L'utilisation d'échantillons de patients atteints de sepsis indique que ce mécanisme de surexpression de ILT4 est perturbé dans un contexte inflammatoire et suggère un impact sur l'activité des neutrophiles au cours de ce syndrome. L'ensemble de ces études nous permet d'envisager les récepteurs ILT2 et ILT4 ainsi que leur ligand HLA-G comme des cibles thérapeutiques dans les traitements de patients atteints de cancers ou comme outils thérapeutiques dans le traitement de pathologies inflammatoiresDisruption or subversion of innate immunity tolerogenic mechanisms can lead to several diseases. On one hand, interaction of ILT2 inhibitory receptor expressed on NK and y8 T cells with HLA-G molecule expressed on tumor cells enable these last to escape from the antitumor activity of these two populations. Indeed, independently from tumor lipid rafts integrity, HLA-G prevents the organisation of NK cells immunological synapse and therefore inhibits their cytolytic activity. Moreover, it induces the inhibition of y5 T cells proliferation, IFN-y synthesis and cytotoxicity. On the other hand, engagement of ILT4, another inhibitory receptor for HLA-G, on neutrophils surface, entails the decrease of both CD32a-dependent phagocytic and oxidative functions. ILT4 is also contained in intracytoplasmic granules and its surface expression can consequently be increased through exocytosis following a pro-inflammatory stimulus. By this way, exocytosis contributes to the regulation of neutrophil activity. The use of sepsis patients' samples indicates that ILT4 up-regulation is disrupted in an inflammatory context and suggests an impact on neutrophils activity in this syndrome. Overall, these studies enable us to propose HLA-G and its receptors ILT2 and ILT4 as new therapeutic targets to optimize immunotherapy treatments for cancer patients or as therapeutic tools in the treatment of inflammatory disorders
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Lesport, Emilie. "Etude des mécanismes d'échappement des tumeurs aux cellules NK et T γδ induits par la molécule HLA-G." Paris 7, 2011. http://www.theses.fr/2011PA077043.
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Les cellules NK et les lymphocytes T γδ constituent deux populations d'effecteurs cytotoxiques impliquées dans le contrôle du développement des tumeurs par le système immunitaire. Cependant, leurs propriétés anti-tumorales peuvent être altérées en raison des mécanismes d'immunosuppression associés aux tumeurs. Dans ce cadre, l'objectif de ma thèse consistait à déterminer comment l'expression de la molécule tolérogène HLA-G par les tumeurs leur permettait d'échapper à la reconnaissance par les cellules NK et les lymphocytes T γδ. Nos résultats ont mis en évidence les mécanismes moléculaires à l'origine de l'inhibition de la cytotoxicité des cellules NK induite par l'expression tumorale de HLA-G. En effet, nous avons démontré que l'interaction entre le récepteur inhibiteur ILT2 et HLA-G inhibe la réorganisation du cytosquelerte d'actine et de tubuline dans la cellule NK, conduisant à un défaut de polarisation des granules cytotoxiques vers la cellule tumorale. Un autre aspect de ma thèse a concerné l'étude du rôle de HLA-G sur les fonctions des lymphocytes T γδ. Nos données indiquent que l'expression de HLA-G par des cellules tumorales primaires inhibe l'activité cytotoxique des lymphocytes T y5 en interagissant avec le récepteur ILT2. De plus, cette expression induit un défaut de production d'IFN-γ ainsi qu'une inhibition de la prolifération des lymphocytes T γδ. L'ensemble de ces données permet de mieux comprendre par quels mécanismes les tumeurs exprimant HLA-G échappent au système immunitaire, et pourrait à terme contribuer à l'optimisation des traitements d'immunothérapie chez les patients atteints de cancer et pour lesquels une expression de HLA-G est observéeNatural Killer (NK) cells and γδ T cells are both cytotoxic effectors playing a major role in the immunosurveillance of cancers. Even though tumors can be eliminated thanks to the potent anti-tumoral fonctions of these immune cells, it is well establish that they develop various mechanisms in order to évade the immune System. In this regard, the aim of my thesis was to understand how the expression of the tolerogenic molécule HLA-G by tumor cells contributes to their escape from NK and γδ T cell recognition. We identified the molecular events leading to the inhibition of NK cell cytotoxicity induced by tumor cells expressing HLA-G. Our results demonstrate that the interaction of the ILT2 inhibitory receptor expressed by NK cells with HLA-G inhibits the reorganization of actin and tubulin cytoskeleton within the NK cells, thus preventing the polarization and the delivery of lytic granules toward the tumor target cells. In parallel, we studied the effect of HLA-G expression by tumor cells on the fonctions of γδ T cells. We showed that primary tumor cells expressing HLA-G are protected against γδ T cell-mediated cytolysis and that this inhibition was due to the interaction of HLA-G with ILT2. Moreover, our data indicate that HLA-G expression by tumor cells inhibits both the production of IFN-y and the proliferation of γδ T cells. Altogether, these results are important for a better understanding of the mechanisms linking HLA-G expression and tumor immune escape. In the future, they could contribute to the optimization of immunotherapy treatments for cancer patients expressing HLA-G
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Bernage, Fabienne. "Virus de l'hépatite D : Etude séro-épidémiologique du virus Delta dans un hôpital de la région parisienne." Paris 5, 1992. http://www.theses.fr/1992PA05P025.
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Abdou, Chekaraou Mariama. "Variabilité génétique des souches virales HBV et HDV circulant dans la région du Sahara en Afrique et étude de la co-spéciation HBV/HDV." Paris 13, 2010. http://www.theses.fr/2010PA132001.
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L’infection par le virus de l’hépatite B (HBV) constitue en Afrique Subsaharienne un problème de santé publique majeur. Le taux de prévalence de la protéine d’enveloppe du virus, l’antigène HBs (AgHBs) peut atteindre jusqu’à 30% dans certains pays. De plus on estime entre 70 à 100 millions le nombre de porteurs chroniques de l’HBV avec une fréquence de décès annuels de l’ordre de 250 000. Les données concernant l’infection concomitante par le virus de l’hépatite D (HDV) virus satellite de l’HBV, sont très rares car très peu d’études ont été conduites. Les génotypes HBV/E, et l’HBV/A ont été identifiés en Afrique subsaharienne, le génotype D étant cantonné à l’Afrique du Nord. De plus, plusieurs souches recombinantes entre le génotype E et les génotypes, A et D ont aussi été décrit. Concernant l’HDV, 4 génotypes « africains », HDV 5, -6, -7 et -8 ont été caractérisés au laboratoire chez des patients africains immigrés en France, infectés dans leur pays d’origine. Au cours de cette étude nous avons voulu déterminer l’épidémiologie moléculaire des souches HBV et HDV circulant au Niger, et plus généralement dans la région du Sahara (Mali de Mauritanie et du Tchad). Au partir d’une cohorte de donneurs de sang du Niger porteurs de l’AgHBs, nous avons retrouvé que 80% des souches étudiées appartenaient au génotype E. Ces souches présentaient une variabilité génétique significativement plus différente que celle décrite pour les souches HBV/E de la littérature (p<0,005) suggérant une diffusion plus ancienne de l’infection au Niger. De plus, nous avons mis en évidence un nouveau recombinant HBV/D-E entre des souches HBV/D et HBV/E, représentant près de 20% des souches isolées de notre cohorte, présentant des points de cassures précis, situés dans des « points chauds » de recombinaison décrits dans la littérature. Ce recombinant HBV/D-E présentait un taux de divergence dans sa séquence nucléotidique complète de plus de 4% en par rapport aux sous génotypes HBV/D décrits à ce jour. Les analyses phylogénétiques extensives effectuées nous permettent de le classer clairement comme un nouveau sous génotype, nous avons proposé HBV/D8. De même, comme décrits aussi par d’autres équipes, nous avons mis en évidence d’autres recombinants HBV-E/D, à la fois au Niger, mais aussi en Mauritanie avec des profils différents les uns des autres, témoignant de la grande variabilité génétique des souches virales dans la région. En revanche, la prévalence de l’infection Delta au Niger semblait a priori faible. Quatre souches de notre cohorte (7,8%), toutes de génotype HDV-1 ont été isolées. L’étude de la co-spéciation HBV/HDV dans cette région de l’Afrique saharienne (Niger, Mali de Mauritanie et du Tchad) a été entreprise à partir de 82 échantillons de la collection des sérums HDV positifs du laboratoire. Le génotype E était associé à tous les génotypes delta présents HDV-1, -5 et -7. De même, une souche HBV/D était aussi capable de s’associer à l’HDV-1 et -5. Afin de tester si l’enveloppement de HDV par HBV était dépendant ou non des génotypes des souches virales, nous avons mis au point un modèle cellulaire in vitro de co-transfection transitoire de plasmides codant la protéine AgHBs et la grande protéine delta. La méthode de mesure consistait en l’évaluation de la formation de particules pseudo-virales. Les résultats préliminaires obtenus à l’aide de HBV/D co-transfecté avec les génotypes HDV-1, HDV-3, HDV-5 et HDV-6 et HDV-7, montrent que HDV-1, mais pas HDV-5, était enveloppé. Grâce à ce modèle, les études seront poursuivies afin d’analyser la capacité d’enveloppement des différents « génotypes delta africains » par le génotype EInfection with hepatitis B (HBV) in SubSaharan Africe is an issue of major public health. The prevalence of the envelope protein of the virus, HBs antigen (HBsAg) can reach up to 30% in some countries. In addition it is estimated between 70 to 100 million, the number of chronic carriers of HBV with an annual death rate of about 250 000. Data on coinfection with hepatitis D (HDV) virus satellite of HBV are very rare because very few studies have been conducted. In terms of molecular characterization of HBV and HDV circulating strains, studies, although partial and conducted with a small number of samples, have been reported. Two HBV genotypes, HBV/E, and HBV/A (with its sub genotypes A1, A2, A3, A4 and A5) have been mainly identified in sub-Saharan Africa. Genotype D is confined to North Africa. In addition, several recombinant strains between genotype E and genotypes A and/or D have also been described. Concerning the HDV, 4 "African genotypes", HDV-5, -6, -7 and -8 have been characterized in the laboratory from African patients immigrants in France, who had been infected in their country of origin. Two studies conducted in Gabon confirmed the presence of HDV genotype-7 and -8. In this study we wanted to determine the molecular epidemiology of HBV and HDV strains circulating in Niger and more generally in the Sahara region, in neighboring countries of Mali from Mauritania and Chad. In a cohort from blood donors in Niger HBsAg carriers, we found that 80% of the studied strains belonged to genotype E. These strains showed genetic variability significantly different from that described for HBV/E strains of the literature (p <0. 005) suggesting an ancient diffusion of infection in Niger. Furthermore, we identified a new recombinant HB /D-E between strains HBV/D and HBV / E, representing nearly 20% of strains isolated in our cohort, with the specific breakpoints located in hotspots recombination described elsewhere in the literature. The recombinant HBV/D-E showed a divergence in its complete nucleotide sequence of more than 4% as compared to HBV genotypes /D described to date. The extensive phylogenetic analyses carried out allow us to classify it as clear as a new genotype, we proposed HBV/D8. Similarly, as also described by other teams, we have highlighted other recombinant HBV/E-D, both in Niger, but also in Mauritania with profiles different from each other, reflecting the high genetic variability of viral strains in the region. In contrast, the prevalence of HDV infection in Niger seemed a priori low. Four strains in our cohort (7. 8%), all classified as genotype HDV-1 were isolated. The study of HBV / HDV co-speciation in this region of Saharan Africa (Niger, Mali, Mauritania and Chad) was undertaken from 82 samples from the laboratory collection of HDV positive serum. Genotype E was associated with all delta genotypes found, HDV -1, -5 and -7. Similarly, HBV/D strain was also able to envelope the HDV-1 and -5. To test whether the envelopment of HDV or HBV was dependent or not on genotypes of virus strains, we developed a cellular in vitro model of transient co-transfection of plasmids encoding the HBsAg protein and large delta protein. The measurement method consisted of evaluating the formation of viral like particles. Preliminary results obtained with HBV/D co-transfected with HDV-1, -3, -5, -6, and -7, showed that HDV-1, but not HDV-5, was wrapped. With this model, studies are continuing to analyze the ability of the genotype E to wrapping different "Delta African genotypes"
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Hourioux, Christophe. "Interactions entre les protéines d'enveloppe et les protéines de capside au cours de la morphogenèse virale : étude comparée du virus de l'hépatite B, de son satellite delta, et du virus de l'immunodéficience humaine de type 1." Tours, 1999. http://www.theses.fr/1999TOUR3307.
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L'objectif de ces travaux était de rechercher pour ces trois virus les domaines de l'enveloppe potentiellement impliqués dans la morphogenèse virale. L'enveloppe du VHB est constituée par trois protéines S, M et L dont les domaines cytosoliques ont été cartographiés en peptides de synthèse. Leur affinité pour des nucléocapsides purifiées a été évaluée par des tests d'interaction de type E. L. I. S. A. Le même type d'étude a été réalisé avec le VHD qui s'enveloppe dans les protéines S, M et L du VHB. Les mécanismes de morphogenèse du VHD ont été étudiés par mesure des interactions protéines-protéines entre le panel de peptides utilisé précédemment pour le VHB et les deux formes delta 24 et delta 27 de l'Ag HD constituant la pseudocapside virale. Pour le VIH-1, l'affinité de particules Pr55Gag immatures a été testée pour 12 peptides chevauchants, couvrant le domaine cytoplasmique de la glycoprotéine d'enveloppe gp41TM et 4 peptides couvrant les domaines cytoplasmiques de protéines HLA-DR connues pour être incorporées dans l'enveloppe virale. Des travaux préliminaires montrent que des peptides présentant une affinité pour les capsides pourraient présenter des perspectives en stratégie antivirale en entrant en compétition avec les protéines d'enveloppe lors des étapes d'assemblage et de sécrétion virale.
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Brichler, Ségolène. "Le virus de l'hépatite delta : implication du stress oxydant, de STAT-3 et de NF-kappaB dans la pathogénèse virale." Paris 5, 2011. http://www.theses.fr/2011PA05T002.
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Le virus de l'hépatite delta (VHD) est un satellite du virus de l’hépatite B (VHB). Il utilise les protéines d’enveloppe de ce dernier pour former ses particules virales. Le génome du VHD code deux protéines, p24 (ou petite protéine sHDAg) et p27 (ou grande protéine LHDAg), à partir d’une seule phase de lecture ouverte située sur l’antigénome, et ce, grâce à un mécanisme d’édition de l’ARN messager. P24 et p27 sont strictement identiques, exceptés pour les 19 acides aminés additionnels en C-terminal de p27, qui contiennent un site d'isoprénylation sur le résidu cystéine en position 211 (C211). Cette isoprénylation est critique pour l’adressage de la ribonucléoprotéine delta à la membrane du réticulum endoplasmique (RE), pour son interaction avec les protéines d'enveloppe du VHB et pour l’assemblage et la sécrétion des virions delta. Au cours de l’infection VHB/VHD, on observe en règle générale une inhibition de la réplication du VHB. Cependant, la maladie hépatique qui en résulte est beaucoup plus grave, avec une plus grande fréquence des formes fulminantes, et surtout une progression accélérée vers la cirrhose et le carcinome hépatocellulaire. Les mécanismes de cette aggravation ne sont pas élucidés, mais suggèrent une pathogenèse spécifique liée au VHD. Afin d’explorer ces questions, nous avons utilisé un modèle de transfection transitoire de cellules hépatocytaires Huh7, à l’aide de plasmides codant les protéines delta p24 et p27. Dans une première étude, nous montrons que p27, et p24 dans une moindre mesure, inhibent la réplication du VHB, en bloquant l’activation des enhancers 1 et 2 responsables du haut niveau de réplication du VHB et de la spécificité hépatocytaire de cette réplication. De plus, nous montrons que p27 est capable d’activer le promoteur du gène codant la protéine antivirale MxA inductible par les interférons de type I (IFNa/b) et de potentialiser l’effet des IFNa/b sur ce promoteur MxA. Dans une seconde étude, nous avons recherché des mécanismes de pathogenèse spécifique liés au VHD, responsables de l’aggravation de la maladie hépatique au cours de l’infection VHB/VHD. L’activation des voies du stress oxydant semble être un mécanisme électif dans la pathogénicité des virus des hépatites B et C (VHC). En effet, les protéines non structurales, NS5A notamment, et la capside du VHC, ainsi que la protéine HBx et les protéines d’enveloppe du VHB, sont capables d’induire un stress oxydant au sein de la cellule. De nombreux facteurs de transcription impliqués dans diverses voies de signalisation cellulaire sont ainsi activés. Parmi ceux-ci, on distingue STAT-3, considéré comme un véritable oncogène, et NF-kB, deux facteurs clefs de la régulation de la prolifération et de la mort cellulaire, dont l’activation a été retrouvée dans de nombreux types de cancers dont l’hépatocarcinome cellulaire. Nos résultats montrent que p27 induit de façon significative un stress du RE, ainsi qu’une augmentation de la synthèse de l’enzyme NADPH oxydase 4 (Nox4), impliqués dans la production en excès de radicaux oxygénés (ROS) dans la cellule et la phosphorylation sur sérine ou thréonine de nombreux facteurs de transcription. Nous montrons en effet dans notre modèle, une production de ROS significativement plus élevée dans les cellules exprimant p27, de même que la phosphorylation et la translocation nucléaire de STAT-3 et de NF-kB. Ces résultats sont confirmés par l’utilisation d’antioxydants et d’inhibiteurs calciques qui inhibent cette activation. De même, en utilisant un plasmide p27 où la C211 est mutée en Sérine, nous avons obtenu une diminution de 50% de l’activation de STAT-3 et de NF-kB confirmant le rôle de l’isoprénylation dans les effets observés. Ainsi, en conclusion, nos résultats constituent une première approche de la compréhension des mécanismes de la pathogenèse hépatique spécifique liée au VHDThe hepatitis delta virus (HDV) is a satellite of hepatitis B virus (HBV). HDV uses the HBV envelope proteins to form its viral particles. The HDV genome encodes two proteins, p24 (or small protein sHDAg) and p27 (or large protein LHDAg) from a single open reading frame located on the antigenome through an editing event occuring on the delta mRNA. P24 and p27 are identical, except for the 19 additional amino acids at p27 Cterminus, which contain an isoprenylation site on a cysteine residue at position 211 (C211). This isoprenylation is critical for addressing the delta ribonucleoprotein to the endoplasmic reticulum (ER) membrane, for interaction with HBV envelope proteins, assembly and secretion of delta virions. During HBV/HDV co-infection, an inhibition of HBV replication is generally observed. However, the resulting liver disease is much more severe, with a higher incidence of fulminant hepatitis, and an accelerated progression to cirrhosis and hepatocellular carcinoma. The mechanisms are unclear, but suggest a specific HDV-related pathogenesis. To explore these questions, we used a transient transfection of Huh7 hepatocytes, using plasmids encoding the p24 and p27 delta proteins. In a first study, we show that p27, and p24 to a lesser extent, inhibit HBV replication by blocking the activation of enhancers 1 and 2, reponsible for the high level of HBV replication. Moreover, p27 can activate the interferon type I (IFNa/b)-inducible MxA promoter, and potentiate the effect of IFNa/b on MxA promoter. In a second study we investigated possible specific pathogenic mechanisms relaed to HDV. The activation of oxidative stress pathways appears to be an elective mechanism in hepatitis B and C (HCV) pathogenesis. Indeed HCV nonstructural NS5A and core proteins, and HBV HBx and envelope proteins, can induce oxidative stress within infected cells. Many transcription factors involved in various cellular signaling pathways are thus activated. Among these, STAT-3, considered as a true oncogene and NF-kB are two key factors regulating proliferation and cell death. Their activation has been found in many types of cancer, including hepatocellular carcinoma. Our results show that p27 induces a significant ER stress and an increased synthesis of the NADPH oxidase 4 (Nox4) enzyme, involved in the overproduction of reactive oxygen species (ROS) in the cell, and serine or threonine phosphorylation of many transcription factors. Indeed, in our model, ROS production is significantly higher in cells expressing p27, as well as phosphorylation and nuclear translocation of STAT-3 and NF-kB. These results are confirmed by the use of antioxidants and calcium inhibitors that strongly inhibit this activation. Similarly, using a p27 plasmid construct in which C211 is mutated to serine, we obtained a 50% decrease of STAT-3 and NF-kB activation, confirming the role of isoprenylation in the observed effects. In conclusion, our results constitute a first approach to understanding the mechanisms of HDV-related liver pathogenesis
Books on the topic "Antigène delta"
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Hepatitis delta virus: Molecular biology, pathogenesis, and clinical aspects : proceedings of the Fourth International Symposium on Heptitis Delta Virus, held at Rhodes, Greece, June 8-10, 1992. New York: Wiley-Liss, 1993.
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Nicola, Giulia Paola Di. Antigone: Figura femminile della trasgressione. Pescara: Edizioni Tracce, 1991.
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Voltaggio, Franco. Antigone tradita: Una contraddizione della modernità : libertà e Stato nazionale. [Rome]: Editori internazionali riuniti, 2013.
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Hepatitis Delta Virus (Current Topics in Microbiology and Immunology). Springer, 2006.
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Pfeffer, Klaus. Function And Specificity Of Gama/delta T Cells (Current Topics in Microbiology & Immunology). Edited by Klaus Pfeffer. Springer, 1991.
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K, Pfeffer, ed. Function and specificity of [alpha/delta] T cells: International Workshop, Schloss Elmau, Bavaria, FRG, October 14-16, 1990. Berlin: Springer, 1991.
Find full textBook chapters on the topic "Antigène delta"
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Ehling, A., B. Gierten, and T. Arndt. "Delta-Antigen." In Springer Reference Medizin, 668–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_844.
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Ehling, A., B. Gierten, and T. Arndt. "delta-Antigen." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_844-1.
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Modlin, Robert L., Julie Lewis, Koichi Uyemura, and Robert E. Tigelaar. "T Lymphocytes Bearing Gamma-Delta Antigen Receptors in Skin." In Heat-Shock Proteins and Gamma-Delta T Cells, 61–74. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319103.
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Christmas, Stephen E. "Cytokine Production by T Lymphocytes Bearing the Gamma-Delta T Cell Antigen Receptor." In Heat-Shock Proteins and Gamma-Delta T Cells, 32–46. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319101.
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Tappero, G., G. Natoli, F. Negro, Antonina Smedile, F. Bonino, M. Rizzetto, and M. Levrero. "Accumulation of a cellular protein bearing c-myc-like antigenicity in hepatic and non-hepatic delta antigen expressing cells." In Research in Chronic Viral Hepatitis, 73–79. Vienna: Springer Vienna, 1993. http://dx.doi.org/10.1007/978-3-7091-9312-9_8.
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"Hepatitis (D)Delta-Antigen." In Springer Reference Medizin, 1098. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_311767.
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"Antikörper gegen Hepatitis-Delta-Virus-Antigen." In Springer Reference Medizin, 158. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_310244.
Full textConference papers on the topic "Antigène delta"
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Ramona, Stoicescu, Stoicescu Razvan-Alexandru, Codrin Gheorghe, and Schroder Verginica. "LABORATORY METHODS AND PREVALENCE OF SARS-COV-2 INFECTIONS IN THE 2ND SEMESTER OF 2021 IN THE EMERGENCY CLINICAL COUNTY HOSPITAL OF CONSTANTA." In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/11.
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"Diagnosing infections with SARS-CoV-2 is still of great interest due to the health and economic impact of COVID pandemic. The 4th wave of the COVID-19 pandemic is expected and is considered to be stronger and faster due to the dominance of Delta variant which is highly contagious [1]. SARS-CoV-2 also known as 2019-nCoV is one of the three coronaviruses (together with SARS-CoV or SARS-CoV1/Severe acute respiratory syndrome coronavirus), MERS-CoV /Middle East Respiratory Syndrome coronavirus) which can cause severe respiratory tract infections in humans [2]. Early diagnosis in COVID 19 infection is the key for preventing infection transmission in collectivity and proper medical care for the ill patients. Gold standard for diagnosing SARS-Co-V-2 infection according to WHO recommendation is using nucleic acid amplification tests (NAAT)/ reverse transcription polymerase chain reaction (RT-PCR). The search is on to develop reliable but less expensive and faster diagnostic tests that detect antigens specific for SARS-CoV-2 infection. Antigen-detection diagnostic tests are designed to directly detect SARSCoV-2 proteins produced by replicating virus in respiratory secretions so-called rapid diagnostic tests, or RDTs. The diagnostic development landscape is dynamic, with nearly a hundred companies developing or manufacturing rapid tests for SARS-CoV-2 antigen detection [3]. In the last 3 months our hospital introduced the antigen test or Rapid diagnostic tests (RDT) which detects the presence of viral proteins (antigens) expressed by the COVID-19 virus in a sample from the respiratory tract of a person. All RDT were confirmed next day with a RT-PCR. The number of positive cases detected during 3 months in our laboratory was 425. There were 326 positive tests in April, 106 positive tests in May and 7 positive tests in June. Compared with the number of positive tests in the 1st semester of 2021, the positive tests have significantly declined."
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Fisher, Jonathan, anna capsomidis, Barry Flutter, Gabriel Benthal, Rebcca Wallace, Kenth Gustafsson, Karin Straathof, Martin Pule, and John Anderson. "Abstract B128: Chimeric antigen receptor transduced gamma delta T lymphocytes provide enhanced tumor specificity." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b128.
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de Silva, Suresh, George Fromm, Anne Lai, Louis Gonzalez, Arpita Patel, Kyung Jin Yoo, Kellsey Johannes, Kinsley Evans, Keith Wilson, and Taylor H. Schreiber. "Abstract 1736: Antigen-specific targeting of tissue-resident gamma delta T cells with recombinant butyrophilin heterodimeric fusion proteins." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1736.
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Fueyo, Juan, Charles Conrad, Candelaria Gomez-Manzano, Amy Heimberger, Luis Vence, Kenneth Aldape, Alfred Yung, Raymond Sawaya, Gregory Fuller, and Frederick Lang. "Abstract LB-123: Analyses of anti-cancer testis antigen antibodies in glioma patients treated with Delta-24 oncolytic adenovirus." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-123.
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