Relevant bibliographies by topics / Antigen CD163

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Academic literature on the topic 'Antigen CD163'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Antigen CD163"

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Costa-Hurtado, Mar, Alexandre Olvera, Verónica Martinez-Moliner, Nuria Galofré-Milà, Paloma Martínez, Javier Dominguez, and Virginia Aragon. "Changes in Macrophage Phenotype after Infection of Pigs with Haemophilus parasuis Strains with Different Levels of Virulence." Infection and Immunity 81, no. 7 (April 15, 2013): 2327–33. http://dx.doi.org/10.1128/iai.00056-13.

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ABSTRACTHaemophilus parasuisis a colonizer of healthy piglets and the etiological agent of Glässer's disease. Differences in virulence among strains ofH. parasuishave been widely observed. In order to explore the host-pathogen interaction, snatch-farrowed colostrum-deprived piglets were intranasally infected with 4 strains ofH. parasuis: reference virulent strain Nagasaki, reference nonvirulent strain SW114, field strain IT29205 (from a systemic lesion and virulent in a previous challenge), and field strain F9 (from the nasal cavity of a healthy piglet). At different times after infection, two animals of each group were euthanized and alveolar macrophages were analyzed for the expression of CD163, CD172a, SLA I (swine histocompatibility leukocyte antigen I), SLA II, sialoadhesin (or CD169), and CD14. At 1 day postinfection (dpi), virulent strains induced reduced expression of CD163, SLA II, and CD172a on the surfaces of the macrophages, while nonvirulent strains induced increased expression of CD163, both compared to noninfected controls. At 2 dpi, the pattern switched into a strong expression of CD172a, CD163, and sialoadhesin by the virulent strains, which was followed by a steep increase in interleukin 8 (IL-8) and soluble CD163 in serum at 3 to 4 dpi. The early increase in surface expression of CD163 induced by nonvirulent strains went along with higher levels of IL-8 in serum than those induced by virulent strains in the first 2 days of infection. Alpha interferon (IFN-α) induction was observed only in animals infected with nonvirulent strains. Overall, these results are compatible with a delay in macrophage activation by virulent strains, which may be critical for disease production.
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Fabriek, Babs O., Machteld M. J. Polfliet, Rianka P. M. Vloet, Roel C. van der Schors, Antoon J. M. Ligtenberg, Lehn K. Weaver, Christiaan Geest, et al. "The macrophage CD163 surface glycoprotein is an erythroblast adhesion receptor." Blood 109, no. 12 (June 15, 2007): 5223–29. http://dx.doi.org/10.1182/blood-2006-08-036467.

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Abstract Erythropoiesis occurs in erythroblastic islands, where developing erythroblasts closely interact with macrophages. The adhesion molecules that govern macrophage-erythroblast contact have only been partially defined. Our previous work has implicated the rat ED2 antigen, which is highly expressed on the surface of macrophages in erythroblastic islands, in erythroblast binding. In particular, the monoclonal antibody ED2 was found to inhibit erythroblast binding to bone marrow macrophages. Here, we identify the ED2 antigen as the rat CD163 surface glycoprotein, a member of the group B scavenger receptor cysteine-rich (SRCR) family that has previously been shown to function as a receptor for hemoglobin-haptoglobin (Hb-Hp) complexes and is believed to contribute to the clearance of free hemoglobin. CD163 transfectants and recombinant protein containing the extracellular domain of CD163 supported the adhesion of erythroblastic cells. Furthermore, we identified a 13–amino acid motif (CD163p2) corresponding to a putative interaction site within the second scavenger receptor domain of CD163 that could mediate erythroblast binding. Finally, CD163p2 promoted erythroid expansion in vitro, suggesting that it enhanced erythroid proliferation and/or survival, but did not affect differentiation. These findings identify CD163 on macrophages as an adhesion receptor for erythroblasts in erythroblastic islands, and suggest a regulatory role for CD163 during erythropoiesis.
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Schaer, D. J., G. Schoedon, and A. Schaffner. "Assignment of the CD163 antigen (Cd163) to mouse chromosome 6 band F2 by radiation hybrid mapping." Cytogenetic and Genome Research 98, no. 2-3 (2002): 231B. http://dx.doi.org/10.1159/000069812.

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Nishiwaki, Satoshi, Seitaro Terakura, Tatsunori Goto, Aika Seto, Keisuke Watanabe, Nobuhiko Imahashi, Shokichi Tsukamoto, et al. "Macrophage Infiltration of Skin Lesions Correlates to Prognosis of Gvhd; A Clue to Refractory Gvhd." Blood 112, no. 11 (November 16, 2008): 1178. http://dx.doi.org/10.1182/blood.v112.11.1178.1178.

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Abstract The pathophysiology of acute graft-versus-host disease (aGVHD) is a complex process. Although it is considered an alloimmune attack on host tissues mounted mainly by donor CD8-positive T cells, skin infiltration of T cells is not always the case in biopsy specimens of skin aGVHD, suggesting the involvement of other cellular components. In detailed observation, CD163-positive macrophages which have abilities of antigen presentation and releasing cytokines were frequently observed. We retrospectively reviewed 66 biopsy specimens of skin lesions clinically thought to be aGVHD performed within 100 days after allogeneic stem cell transplantation, and analyzed the relationship between types of infiltrating cells and clinical outcomes. Paraffin-section immunohistochemical analysis was performed using a monoclonal antibody against CD8 and CD163. Counting the total number of CD8-positive T cells and CD163-positive macrophages in 4 fields with 200-fold magnification, median number of CD-8 positive T cells was 78.5 (range; 2–305), and that of CD163-positive macrophages was 149 (range; 38–372). Infiltration of over 100 cells of CD8-positive T cells (CD8ov100) correlated with HLA class I mismatch and grade III–IV a GVHD, while infiltration of over 200 cells of CD163-positive macrophages (CD163ov200) correlated with grade III–IV aGVHD and refractory aGVHD. In logistic analyses, CD163ov200 (Odds 6.29 (95%CI 1.57–25.0); p=0.009) was identified as the only negative predictors of aGHVD outcome. Overall survival of patients with CD163ov200 was significantly lower than that of those with infiltration of under 200 cells of CD163-positive macrophages (63.0% vs. 40.6% at 1 year, respectively; p=0.02). In 23 patients treated with steroid for aGVHD, CD163ov200 was the only significant predictor of refractory aGVHD outcome (Odds 10.9 (95%CI 1.37–83.3); p=0.02), and overall survival of patients with CD163ov200 was significantly lower than that of those with infiltration of under 200 cells of CD163-positive macrophages (63.5% vs. 12.5% at 1 year, respectively; p=0.0004). These results indicate that CD163-positive macrophages may provide a clue for the pathophysiology of refractory GVHD and new treatment strategies.
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Santegoets, Saskia J., Chantal L. Duurland, Ekaterina J. Jordanova, Vanessa J. van Ham, Ilina Ehsan, Nikki M. Loof, Vipin Narang, et al. "CD163+ cytokine-producing cDC2 stimulate intratumoral type 1 T cell responses in HPV16-induced oropharyngeal cancer." Journal for ImmunoTherapy of Cancer 8, no. 2 (August 2020): e001053. http://dx.doi.org/10.1136/jitc-2020-001053.

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BackgroundHuman papillomavirus (HPV)-associated oropharyngeal squamous cell carcinoma (OPSCC) is a distinct clinical entity with a much better prognosis after (chemo)radiotherapy than HPV-negative OPSCC, especially in patients with a concomitant intratumoral HPV-specific and type-1 cytokine-oriented T cell response. However, knowledge on the type of myeloid cells and their coordination with intratumoral T cells and influence on patient outcome in OPSCC is lacking.MethodsWe analyzed the presence of intratumoral myeloid cells and their relationship to tumor-infiltrating T cells and patient outcome in a well-described cohort of HPV16+ patients with OPSCC using multispectral immunofluorescence, flow cytometry and functional analyses.ResultsWe show that the tumor microenvironment of HPV16+ OPSCC tumors with such an ongoing HPV16-specific T cell response is highly infiltrated with a newly defined CD163+ cytokine-producing subset of conventional dendritic cell type 2 (cDC2), called DC3. These CD163+ cDC2 predominantly stimulated type 1 T cell polarization and produced high levels of interleukin-12 (IL-12) and IL-18, required for IFNγ and IL-22 production by T cells after cognate antigen stimulation. Tumor-infiltration with these CD163+ cDC2 positively correlated with the infiltration by Tbet+ and tumor-specific T cells, and with prolonged survival.ConclusionsThese data suggest an important role for intratumoral CD163+ cDC2 in stimulating tumor-infiltrating T cells to exert their antitumor effects.
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Gandhi, Maher K., David Arpon, Colm Keane, Erica Han, Josh Tobin, Robert Bird, Mark S. Hertzberg, et al. "A Novel Anti-Lymphoma Immune Evasion Mediated By the Interaction Between PD-1 Enriched NK-Cells and CD163+PD-L1+PD-L2+ Tumor Associated Macrophages, That Is More Prominent in Hodgkin Lymphoma Than Diffuse Large B-Cell Lymphoma." Blood 128, no. 22 (December 2, 2016): 918. http://dx.doi.org/10.1182/blood.v128.22.918.918.

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Abstract PD-L1/PD-L2 are immunomodulatory molecules that engage with the PD-1 receptor on immune effector T and NK-cells to inhibit anti-lymphoma immunity. PD-1/PD-L1/PD-L2 axis molecules are prognostic in Hodgkin Lymphoma (HL, Roemer et al J Clin Oncol 2016) and Diffuse Large B-cell Lymphoma (DLBCL, Keane et al Lancet Haem 2015). Importantly, blockade of the axis is associated with particularly potent clinical responses in relapsed/refractory HL (Ansell et al NEJM 2015), as well as response in DLBCL (Armand et al J Clin Oncol 2013). Focus has been on the interaction of PD-L1 on malignant B-cells with PD-1 on HLA-class I restricted CD8+ effector T-cells. This is despite considerable evidence that: A) malignant B-cells in HL and DLBCL frequently lack the ability to present HLA-class I due to mutations in b2M and associated antigen presenting molecules (Challa-Malladi et al Cancer Cell 2013). This makes them insensitive to direct lysis by CD8+ T-cells (Zaretsky et al NEJM 2016) but potentially enhances their sensitivity to NK-cells; B) PD-L1/PD-L2 are expressed by inhibitory CD163+ monocytes/macrophages as well as by malignant B-cells (Chen et al CCR 2013). Here, we seek to establish the contribution of NK-cells and inhibitory CD163+ expressing monocytes/macrophages in the setting of HL and DLBCL. CD163/PD-1/PD-L1/PD-L2 gene expression was quantified by nanoString in 194 patients and was elevated in HL relative to DLBCL tissues (P<0.01, <0.01, <0.0001, <0.0001 respectively). By FACS, intratumoral tumor associated macrophages (TAMs) demonstrate pronounced protein expression of PD-L1/PD-L2 within HL and DLBCL diseased lymph nodes (Fig A). Pre-therapy blood was tested in 114 patients. Interestingly levels in each of total monocytes, CD14+HLA-DRlo monocytoid derived suppressor cells (moMDSC) and CD163+CD14+ monocytes were equivalent between lymphoma sub-types. However, consistent with tissue findings, there was marked increase in PD-L1 expression on CD14+ monocytes, moMDSC and CD163+CD14+ monocytes in HL compared to DLBCL patients (P<0.001, <0.0001 and 0.0086 respectively). The NK-cell marker CD56 were higher in HL compared to DLBCL tissues (P<0.0001). Levels of PD-1 on circulating NK-cells were 7-fold elevated in HL relative to DLBCL (P<0.0001), whereas CD4+ and CD8+ T-cell PD-1 levels were equivalent between lymphoma sub-types. NK-cells can be subdivided into CD3-CD56dimCD16+ and CD3-CD56hiCD16- subsets. The CD16- subset produces abundant cytokines but are only weakly cytotoxic before activation. Although CD16- NK-cells are typically <10% of all NK-cells in the healthy circulation, we show their relative proportion is markedly expanded by 3.5-fold in HL patients. This is of particular importance since CD16- NK-cells are enriched in secondary lymphoid tissues, i.e. the context in which lymphoma resides. Notably, CD3-CD56hiCD16- NK-cells had substantially higher PD-1 expression relative to CD3-CD56dimCD16+ cells (P<0.0001, Fig B). A similarly aberrant NK-cell phenotype was observed in DLBCL. An in-vitro functional model of TAM-like monocytes was developed to demonstrate the potential impact of inhibitory CD163+ expressing monocytes/macrophages on NK-cells in HL and DLBCL. Monocytes were cultured with the M6 TAM inducing cytokine cocktail of M-CSF and IL-6. Consistent with an inhibitory phenotype, M6 cultured monocytes were highly enriched for CD163 (P<0.001) and PD-L1 (P=0.0024). Critically, M6 cultured monocytes suppressed activation of primary NK-cells in direct cytotoxicity and ADCC assays against lymphoma targets. In line with these findings, depletion of circulating monocytes from the blood of pre-therapy HL and DLBCL patients enhanced NK-cell activation relative to monocyte intact PBMC, whereas this was not observed in age/gender-matched healthy control participants. Interestingly, the increase in NK-cell activation following monocyte depletion was most pronounced in the CD16-CD56hiCD3- NK-cell subset. We describe a hitherto unrecognised immune evasion strategy mediated via skewing towards an exhausted PD-1 enriched CD16-CD56hiCD3- NK-cell phenotype. In addition to inhibition of NK-cells by the malignant B-cell, suppression of NK-cells occurs by PD-L1/PD-L2 expressing tumor associated macrophages. This mechanism is more prominent in HL than DLBCL. Figure. Figure. Disclosures No relevant conflicts of interest to declare.
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Sánchez-Martín, Lorena, Ana Estecha, Rafael Samaniego, Silvia Sánchez-Ramón, Miguel Ángel Vega, and Paloma Sánchez-Mateos. "The chemokine CXCL12 regulates monocyte-macrophage differentiation and RUNX3 expression." Blood 117, no. 1 (January 6, 2011): 88–97. http://dx.doi.org/10.1182/blood-2009-12-258186.

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Abstract Monocytes are versatile cells that can express different functional programs in response to microenvironmental signals. We show that primary blood monocytes secrete the CXCL12 chemokine, and express the CXCR4 and CXCR7 receptors, leading to an autocrine/paracrine loop that contribute to shape monocyte differentiation to a distinct type of macrophages, with an enhanced expression of CD4, CD14, and CD163, or dendritic cells, with a reduced functional ability to stimulate antigen-specific T-lymphocyte responses. The in vivo relevance of CXCL12 production by mononuclear phagocytes was studied in metastatic melanoma tissues by a thoroughly immunofluorescence phenotyping of CXCL12high expressing cells, which were CD45+, coexpressed the macrophage antigens CD68, CD163, and CD209 and constituted the 60%-90% of tumor-associated macrophages. Microarray analysis of primary monocytes revealed that the vascular endothelial growth factor and the angiogenic chemokine CCL1 mRNA levels were up-regulated in response to CXCL12, leading to enhanced expression of both proteins. In addition, we found that CXCL12 autocrine/paracrine signaling down-regulates the expression of the transcription factor RUNX3 and contributes to maintain the long-term CD4 and CD14 expression in monocytes/macrophages. Together, these results suggest that autocrine CXCL12 production modulates differentiation of monocytes toward a distinct program with proangiogenic and immunosuppressive functions.
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Sun, Zhaoyu, Richard Nyberg, Yaping Wu, Brady Bernard, and William L. Redmond. "Developing an enhanced 7-color multiplex IHC protocol to dissect immune infiltration in human cancers." PLOS ONE 16, no. 2 (February 17, 2021): e0247238. http://dx.doi.org/10.1371/journal.pone.0247238.

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The TSA Opal multiplex immunohistochemistry (mIHC) protocol (PerkinElmer) has been used to characterize immune infiltration in human cancers. This technique allows multiple biomarkers to be simultaneously stained in a single tissue section, which helps to elucidate the spatial relationship among individual cell types. We developed and optimized two improved mIHC protocols for a 7-color panel containing 6 biomarkers (CD3, CD8, CD163, PD-L1, FoxP3, and cytokeratin (CK)) and DAPI. The only difference between these two protocols was the staining sequence of those 6 biomarkers as the first sequence is PD-L1/CD163/CD8/CK/CD3/FoxP3/DAPI and the second sequence is FoxP3/CD163/CD8/CK/CD3/PD-L1/DAPI. By comparing PD-L1/FoxP3 staining in mIHC and singleplex PD-L1/FoxP3 staining on the adjacent slide, we demonstrated that the staining sequence does not affect the staining intensity of individual biomarkers as long as a proper antigen retrieval method was used. Our study suggests that use of an antigen retrieval buffer with higher pH value (such as Tris-EDTA pH9.0) than that of the stripping buffers (such as citrate buffer pH6.0) is helpful when using this advanced mIHC method to develop panels with multiple biomarkers. Otherwise, individual biomarkers may exhibit different intensities when the staining sequence is changed. By using this protocol, we characterized immune infiltration and PD-L1 expression in head and neck squamous cell carcinoma (HNSCC), breast cancer (BCa), and non-small cell lung cancer (NSCLC) specimens. We observed a statistically significant increase in CD3+ cell populations within the stroma of NSCLC as compared to BCa and increased PD-L1+ tumor cells in HNSCC as opposed to BCa.
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Gemei, Marica, Rosa Di Noto, Peppino Mirabelli, and Luigi Del Vecchio. "Cytometric Profiling of CD133+ Cells in Human Colon Carcinoma Cell Lines Identifies a Common core Phenotype and Cell Type-specific Mosaics." International Journal of Biological Markers 28, no. 3 (July 2013): 267–73. http://dx.doi.org/10.5301/jbm.5000020.

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In colorectal cancer, CD133+ cells from fresh biopsies proved to be more tumorigenic than their CD133– counterparts. Nevertheless, the function of CD133 protein in tumorigenic cells seems only marginal. Moreover, CD133 expression alone is insufficient to isolate true cancer stem cells, since only 1 out of 262 CD133+ cells actually displays stem-cell capacity. Thus, new markers for colorectal cancer stem cells are needed. Here, we show the extensive characterization of CD133+ cells in 5 different colon carcinoma continuous cell lines (HT29, HCT116, Caco2, GEO and LS174T), each representing a different maturation level of colorectal cancer cells. Markers associated with stemness, tumorigenesis and metastatic potential were selected. We identified 6 molecules consistently present on CD133+ cells: CD9, CD29, CD49b, CD59, CD151, and CD326. By contrast, CD24, CD26, CD54, CD66c, CD81, CD90, CD99, CD112, CD164, CD166, and CD200 showed a discontinuous behavior, which led us to identify cell type-specific surface antigen mosaics. Finally, some antigens, e.g. CD227, indicated the possibility of classifying the CD133+ cells into 2 subsets likely exhibiting specific features. This study reports, for the first time, an extended characterization of the CD133+ cells in colon carcinoma cell lines and provides a “dictionary” of antigens to be used in colorectal cancer research.
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Poderoso, Teresa, Paloma Martínez, Belén Álvarez, Ana Handler, Sara Moreno, Fernando Alonso, Ángel Ezquerra, Javier Domínguez, and Concepción Revilla. "Delivery of antigen to sialoadhesin or CD163 improves the specific immune response in pigs." Vaccine 29, no. 29-30 (June 2011): 4813–20. http://dx.doi.org/10.1016/j.vaccine.2011.04.076.

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Dissertations / Theses on the topic "Antigen CD163"

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Petersen, Sven Hans. "The role of Tetraspanin CD63 in antigen presentation to CD4+ T cells." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1709/.

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CD4+ T cells play a key role in orchestrating adaptive immunity. Their activation requires antigen presentation via MHC II proteins on antigen presenting cells (APC). Exosomes are membrane vesicles released by various cell types including APCs. APC-derived exosomes are MHC class II-positive and can induce CD4+ T cell responses. MHC II delivery to the cell surface and/or exosomes might be influenced by tetraspanins, a family of transmembrane proteins. We have prepared exosomes derived from Epstein-Barr virus (EBV)-infected human B lymphoblastoid cell lines (LCLs) and shown by Western blotting and immunoelectron microscopy that they contain MHC class II and tetraspanins including CD63, CD81 and CD82. Such LCLs as well as LCL-derived exosomes can mediate immunologically specific recognition by MHC class II matched EBV antigen-specific CD4+ T cell clones when directly added to the T cells. Using shRNA, we have decreased CD63 expression in LCLs and had been studying the effect of such downregulation on LCL as well as LCL-derived exosome mediated antigen presentation. Despite an unaltered level of MHC II, CD63low LCLs showed to be hyperstimulatory. In spite of a similar depletion of CD63 in exosomes derived from CD63low LCLs, the CD4+ T cell stimulation by these exosomes was unaltered. In search for the mechanism of this phenomenon we found a higher level of exosome secretion by CD63low LCLs. We speculate that CD63 may influence T cell stimulation by exosome trafficking as well as exosome release.
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Bernatchez, Emilie. "CD103-mediated regulation of airway hypersensitivity responses to bioaerosol-associated antigens." Doctoral thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/30253.

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Les mécanismes immunitaires impliqués dans le maintien de l’homéostasie pulmonaire sont finement régulés étant donné l’exposition constante des voies aériennes aux bioaérosols. Plusieurs cellules participent au maintien de l’homéostasie pulmonaire, telles les cellules dendritiques. Un sous-type de cellules dendritiques pulmonaires attire particulièrement l’attention dans l’homéostasie pulmonaire, les cellules dendritiques CD103+, étant donné qu’il a été démontré qu’elles participent dans la tolérance immune. Toutefois, ce rôle reste controversé, car des études démontrent qu’elles participent plutôt au développement de réponses inflammatoires pulmonaires. De plus, le CD103 (une intégrine exprimée par des sous-types de cellules dendritiques et de lymphocytes T), est surtout utilisé comme marqueur cellulaire et le rôle spécifique joué par l’expression du CD103 sur ces cellules reste inconnu. L’homéostasie pulmonaire n’est pas toujours maintenue. Chez des individus susceptibles, l’exposition aux bioaérosols peut mener au développement de réponses inflammatoires. C’est le cas pour l’asthme et l’alvéolite allergique extrinsèque, deux réponses d’hypersensibilités pulmonaires, de type I et de type mixte III/IV respectivement. Récemment, des espèces d’archées, Methanosphaera stadtmanae (MSS) et Methanobrevibacter smithii (MBS), ont été retrouvées en grande concentration dans les bioaérosols d’environnements agricoles et il a été démontré que l’exposition pulmonaire à leur extrait mène au développement d’une réponse immune chez la souris. Toutefois, le type de réponse d’hypersensibilité pulmonaire qu’elles induisent reste méconnu, une information cruciale qui permettra la poursuite de la recherche sur leur potentiel d’induire une réponse pulmonaire chez l’humain. De plus, même si plusieurs thérapies contre les maladies d’hypersensibilité pulmonaires existent, ce ne sont pas tous les sous-groupes de patients qui répondent à la médication, menant à des conséquences socio-économiques importantes pour le système de santé et pour les patients. Ainsi, il demeure important de poursuivre la recherche sur de potentielles cibles thérapeutiques, telles les cellules impliquées dans le maintien de l’homéostasie pulmonaire. Cette thèse vise donc à évaluer le rôle de l’expression du CD103 dans le maintien de l’homéostasie pulmonaire dans le contexte de maladies d’hypersensibilité pulmonaires induites par des antigènes retrouvés dans les bioaérosols. Le rôle de l’expression du CD103 dans l’hypersensibilité de type I induite par l’ovalbumine ou l’extrait d’acariens (modèles d’asthme) a d’abord été a évalué via l’utilisation de souris Cd103-/-. Nous démontrons que l’expression du CD103 est cruciale pour le contrôle de la sévérité de l’inflammation pulmonaire et qu’elle pourrait être impliquée dans l’initiation de la phase de résolution de la réponse inflammatoire. De plus, l’expression du CD103 sur les cellules dendritiques joue un rôle dans leur migration aux ganglions lymphatiques. Ensuite, nous avons évalué le rôle de l’expression du CD103 dans la réponse d’hypersensibilité de type mixte III/IV en réponse à Saccharopolyspora rectivirgula (SR; modèle d’alvéolite allergique extrinsèque) en utilisant des souris Cd103-/-. De plus, en utilisant des modèles de transfert de cellules, nous avons évalué le rôle de l’expression du CD103 dans la réponse au SR lorsque seulement exprimé par les cellules dendritiques ou seulement par les lymphocytes T CD4. Nous démontrons que c’est l’expression du CD103 sur les cellules dendritiques spécifiquement qui est impliquée dans la régulation de l’initiation de la réponse inflammatoire. Après avoir déterminé le type de réponse d’hypersensibilité induite par l’extrait de MSS ou MBS, nous avons étudié le rôle de l’expression du CD103 en réponse à ces archées. Nous démontrons que l’exposition à MSS induit une réponse immune typique d’une hypersensibilité pulmonaire de type IV. Les résultats obtenus après l’exposition à MBS indiquent aussi que la réponse développée est une hypersensibilité de type IV, même si cela reste à confirmer. Finalement, étant donné une grande variabilité entre nos expériences chez les souris Cd103-/-, nous n’avons pu obtenir de conclusion sur le rôle de l’expression du CD103 dans les réponses d’hypersensibilités induites par les archées. Ces résultats démontrent que l’expression du CD103 sur les cellules dendritiques joue un rôle dans le contrôle de l’homéostasie pulmonaire en réponse à des bioaérosols spécifiques qui induisent une hypersensibilité pulmonaire. Les mécanismes exacts régulés par le CD103 sur les cellules dendritiques menant au maintien de l’homéostasie pulmonaire restent à être élucidé. De plus, nos résultats confirment que les espèces d’archées MSS et MBS induisent chacune une réponse d’hypersensibilité pulmonaire qui lui est spécifique, des résultats qui contribueront à déterminer si ces microorganismes induisent une pathologie chez l’Homme.
As we breathe, the lungs are constantly exposed to bioaerosols that challenge the maintenance of airway homeostasis. Many cells are involved in the maintenance of lung homeostasis, such as airway dendritic cells (DCs). A subset of airway DCs has gained special interest in the past years for its role in immune tolerance: CD103+ DCs. Yet, this role remains controversial as there are also reports that they induce airway inflammatory responses. Furthermore, CD103 (an integrin expressed by subsets of DCs and T cells) is mostly used as a marker and whether CD103 expression on these cells plays a specific role remains unknown. Airway homeostasis is not always maintained. Exposure to bioaerosols can elicit an immune response in susceptible individuals, such as in asthma and hypersensitivity pneumonitis, two common airway hypersensitivity diseases of type I and mixed type III/IV hypersensitivity, respectively. Recently, archaea species Methanosphaera stadtmanae (MSS) and Methanobrevibacter smithii (MBS) were identified in high concentrations in bioaerosols from agricultural environments and their extracts were shown to induce an immune response in the airways of mice. However, the type of airway hypersensitivity response they induce remains unknown, a key information that is required if research is pursued on whether they elicit an airway hypersensitivity response in humans. Furthermore, although many therapies for airway hypersensitivity diseases exist, not all subsets of patients respond to the current medication, resulting in high social and economic impacts on the health system and patients. Therefore, research on potential therapy targets for airway hypersensitivity diseases, such as those involved in the maintenance of airway homeostasis, remains important. This thesis focuses on the role of CD103 expression in the maintenance of lung homeostasis in the context of airway hypersensitivity responses induced by antigens found in bioaerosols. We first assessed the role of CD103 expression in type I hypersensitivity in response to ovalbumin or house dust mite extract (models of experimental asthma) using Cd103-/- mice. We found that CD103 expression is crucial in controlling the severity of airway inflammation and could be involved in initiating the resolution of the inflammatory response. Furthermore, CD103 expression on DCs regulates DC trafficking to the draining lymph nodes. We then assessed the role for CD103 expression in mixed type III/IV hypersensitivity in response to Saccharopolyspora rectivirgula extract (SR; model of experimental hypersensitivity pneumonitis) using Cd103-/- mice. Furthermore, using models of cell transfers, we evaluated the role for CD103 expression in the response to SR when specifically expressed by dendritic cells or specifically by CD4 T cells. We demonstrate that CD103 expression on DCs specifically is involved in regulating the onset of the inflammatory response. We finally studied the role for CD103 expression in response to the airway exposure of MSS and MBS extracts, after elucidating the type of hypersensitivity response they induce. We demonstrate that exposure to MSS induces a typical type IV hypersensitivity response. The results obtained after exposure to MBS also indicate development of a type IV hypersensitivity response, although it remains to be confirmed. Finally, due to high variability in the results using Cd103-/- mice, we were unable to reach a conclusion on the role for CD103 expression in response to archaea species. These results demonstrate that CD103 expression by DCs is involved in the control of airway homeostasis to specific airway hypersensitivity-inducing bioaerosols. The exact mechanisms regulated by CD103 on DCs leading to the maintenance of airway homeostasis remain to be elucidated. Furthermore, our results confirm that archaea species MSS and MBS induce a specific type of hypersensitivity response, which will contribute to the elucidation of whether they induce an airway pathology in humans.
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Tusell, Sonia M. "Coronavirus receptors and host range /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 198-221). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Tachet, des Combes Anne. "Etude de la fixation de CD16 soluble sue les plasmocytes malins : optimisation des conditions expérimentales." Paris 5, 1995. http://www.theses.fr/1995PA05P164.

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Allen, Frederick Jr. "CCL3 Augments Antitumor Responses in CT26 by Enhancing Cellular Trafficking and Interferon-Gamma Expression." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1513124234665339.

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Asang, Florian [Verfasser], and Sebastian [Akademischer Betreuer] Kobold. "Antikörper-abhängige Erkennung von humanen Pankreaskarzinom-, Lymphom- und Melanomzellen durch CD16-chimärer Antigen-Rezeptor-modifizierte T-Zellen in vitro / Florian Asang ; Betreuer: Sebastian Kobold." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2021. http://d-nb.info/1228787301/34.

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Korneychuk, Natalia. "Analysis of the roles of Interleukin 15 and CD4+ T cells specific of a dietary antigen in a mouse model of celiac-like enteropathy." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T037/document.

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Dans les conditions physiologiques des robustes mécanismes immunologiques empêchent le développement des réponses exagérées aux antigènes alimentaires. En revanche, dans le cas de maladie céliaque, qui affecte environ 1% de la population occidentale, l’exposition au gluten alimentaire d’individus génétiquement prédisposés HLA-DQ2.5/DQ8 provoque l’entéropathie chronique de l’intestin grêle. Les études précédentes chez l’homme ont établi le rôle crucial de la réponse cellulaire T CD4+ restreinte par HLA-DQ2.5/DQ8 et spécifique du gluten. La réponse T CD4+ est nécessaire mais cependant insuffisante pour induire des lésions tissulaires. D’autres études ont suggéré le rôle de l’interleukine 15 (IL-15). Ainsi, l’IL-15 surexprimée dans la muqueuse des patients céliaques peut interférer avec les mécanismes d’immunorégulation et stimuler l’activation des lymphocytes intraépithéliaux T CD8+ cytotoxiques probablement induisant des lésions épithéliales. Comment les cellules T CD4+ spécifiques du gluten et l’IL-15 interagissent pour activer les lymphocytes intraépithéliaux T CD8+ et induisent des lésions n’a pas été toutefois établi. Pour répondre à cette question, nous avons créé un modèle murin basé en croisant des souris OTII possédant des cellules T CD4+ spécifiques de l’antigène modèle, ovalbumine, avec les souris transgéniques hétérozygotes surexprimant une forme secrétée de l’IL-15 humaine dans l’épithélium intestinale (souris hIL-15Tge). Les souris obtenues OTII+/- B6 and OTII+/- hIL-15Tge+/- ont été mises au régime riche en ovalbumine depuis la période prénatale jusqu’à l’âge de 3 mois. Les souris OTII+/- hIL-15Tge+/-, contrairement aux souris OTII+/- B6, exposées de façon chronique à l’ovalbumine ont développé un retard de croissance et une atrophie villositaire associée à l’expansion des cellules intestinales T CD8+ cytotoxiques, comme dans la maladie céliaque. En outre, nous avons démontré que l’IL-15 altérait l’immunorégulation par les cellules T FoxpP3+ et coopérait avec l’IL-2, produite par les cellules T CD4+ activées par l’OVA, pour l’expansion des cellules T CD8+ non-spécifiques de l’OVA. Nous suggérons que le scénario similaire pourrait opérer dans la maladie céliaque. Au cours de cette étude, j’ai observé que la surexpression chronique de l’IL-15 était associée avec l’expansion de cellules dendritiques CD103+CD11c+CD11b-. Dans la partie de résultats supplémentaires, j’ai démontré que cet effet dépend de la production de la cytokine GM-CSF secrétée par les cellules Natural Killer (NK) activées par l’IL-15 et que ces cellules dendritiques étaient enrichies en cellules CD103+ ayant une capacité accrue de cross-présentation in vitro. Ces derniers résultats illustrent comment l’IL-15 peut moduler les réponses immunes adaptatives en orchestrant la coopération entre les cellules NK et les phagocytes mononucléaires
In physiological conditions, robust immunological mechanisms avoid adverse responses to food antigens. In contrast, in celiac disease that affects about 1% of Western populations, exposure to dietary gluten of genetically predisposed HLA-DQ2.5/ DQ8 individuals triggers a chronic small intestinal enteropathy. Previous studies in humans have established the crucial role of HLA-DQ2/DQ8 restricted gluten-specific intestinal CD4 T cell response. This CD4 T cell response is necessary but is however not sufficient to induce tissue damage. Other studies have pointed to the role of interleukin 15 (IL-15). Thus, IL-15 over-expressed in the mucosa of celiac patients can interfere with immunoregulatory mechanisms and stimulate the activation of cytotoxic CD8 T intraepithelial lymphocytes, thought to induce epithelial lesions. Whether and how gluten-specific CD4 T cells and IL-15 interact to activate CD8 T intraepithelial lymphocytes and to drive intestinal tissue damage has not been however established. To address this question, we have set up a mouse model based on the breeding of OTII mice possessing CD4 T cells specific of a model antigen, ovalbumin, with heterozygous transgenic mice overexpressing a secreted form of human IL-15 in intestinal epithelium (hIL-15Tge mice). Resulting OTII+/- B6 and OTII+/- hIL-15Tge+/- mice were exposed to dietary ovalbumin from the prenatal period until 3 months of age. Upon chronic exposure to ovalbumin, OTII+/- hIL-15Tge+ mice, contrary to their OTII+/- B6 littermates, developed growth retardation, and villous atrophy associated with expansion of intestinal cytotoxic CD8 T cells, as in celiac disease. Moreover, we showed that IL-15 impaired immunoregulation by FoxP3+ T cells and cooperated with IL-2 produced by OVA-activated CD4 T cells to stimulate the expansion of non-cognate cytotoxic CD8 T cells. We suggest that a comparable scenario can operate in celiac disease. During this study, I observed that chronic overexpression of IL-15 was associated with an expansion of CD103+CD11c+CD11b- mononuclear cells. In the Supplementary results, I have shown that this effect depends on the production of GM-CSF secreted by IL-15-activated NK cells and that CD11c+ DCs differentiated in mice overexpressing IL-15 were enriched in CD103+ cells and displayed enhanced cross-presentation abilities in vitro. The latter results illustrate how IL-15, by orchestrating a crosstalk between NK cells and mononuclear phagocytes, can modulate adaptive immune responses
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Pasquier, Adrien. "Lysosomal degradation of insulin granules promotes β-cell failure in type 2 diabetes." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ083/document.

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Notre équipe a récemment découvert l’importance du ciblage des granules d’insuline aux lysosomes lors d’une mise à jeun chez les cellules pancréatiques β. Le diabète de type 2 (TD2) est caractérisé par la résistance à l’insuline couplé au dysfonctionnement des cellules β-et à leur perte. Je souhaitais évaluer le ciblage des granules d’insuline aux lysosomes dans le contexte diabétique. Grâce à un modèle murin, nous avons trouvé que le nombre des lysosomes contenant des granules d’insuline était augmenté chez les cellules β-provenant de souris diabétiques en comparaison aux contrôles. Ceci était accompagné par l’augmentation des niveaux de la protéine lysosomale CD63. Parce que PKD1 contrôle le ciblage des granules d’insuline aux lysosomes lors d’une mise à jeun, nous nous sommes demandé si PKD1 était importante lors d’un diabète de type 2. Dans nos modèles, les niveaux de PKD1 étaient diminués en conditions diabétiques en comparaison aux contrôles. De plus, l’inhibition de PKD1 entrainait l’augmentation du ciblage des granules d’insuline aux lysosomes et accélérait l’apparition du diabète dans notre modèle murin. Nous souhaitions ensuite savoir si l’activation de PKD1 dans les cellules pancréatiques β-pouvait être avantageuse dans un contexte diabétique. De fait, grâce à l’utilisation d’un composé spécifique, nous avons pu montrer que l’activation de PKD1 menait à l’augmentation des niveaux d’insuline sur des ilots pancréatiques humains et ralentissait l’apparition du diabète dans notre modèle murin. Pour conclure, j’ai aussi débuté la caractérisation des lysosomes sur d’autres types cellulaires des ilots pancréatiques. Nous avons observé que LIMP2, une autre protéine lysosomale, était fortement exprimée chez les cellules pancréatiques α
Our team recently uncovered the importance of the targeting of insulin granules to the lysosomal compartments in pancreatic β-cells during fasting. Type 2 Diabetes (T2D) is characterised by insulin resistance coupled with pancreatic β-cell failure which account for both β-cells dysfunction and β-cells death. I wanted to assess the targeting of insulin granule to the lysosomes in the context of T2D. Using murine diabetic model, we found that the number Granule-containing Lysosomes was enhanced in diabetic β-cells in comparison to controls. This was accompanied by an increase in the level of the lysosomal protein CD63. Because PKD1 controls the targeting of insulin granule to the lysosomes during fasting, I wondered if PKD1 was important during T2D. PKD1 levels were decreased in our diabetic models in comparison to controls. Moreover inhibition of PKD1 led to enhanced targeting of the insulin granules to the lysosomes and accelerated apparition of diabetes in our murine model. I also tested if activation of PKD1 in pancreatic β-cells could be beneficial in the context of diabetes. Indeed using a specific compound, we showed that PKD1 activation led to an increase in insulin levels and delayed onset of diabetes in our murine model. My work thus uncovered mechanisms underlying a fundamentally new process in β-cells with potential implications for novel therapeutic directions in T2D. Finally, I started to assess lysosomes in another pancreatic islets cell type. I found that LIMP2, another lysosomal membrane protein, was specifically highly expressed in the pancreatic α-cells
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Misumi, Denise Shimbo. "Validação do Teste de ativação de basófilos no diagnóstico de reações de hipersensibilidade a anti-inflamatórios não esteroidais." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-24062013-152145/.

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Introdução: Atualmente, o diagnóstico das reações de hipersensibilidade a anti-inflamatórios não esteroidais (AINEs) baseia-se na história relatada pelo paciente e, em determinados casos, é realizado o Teste de Provocação. Todavia, este teste pode expor os pacientes a riscos graves, inclusive anafilaxia. Em busca de ferramenta mais segura, tem-se estudado o Teste de Ativação de Basófilos (BAT). Trata-se de um teste in vitro, no qual é possível testar diversos estímulos em uma única amostra de sangue, avaliando a ativação dos basófilos (indicativo de reação de hipersensibilidade), através do aumento da expressão de moléculas na superfície desses leucócitos, como o CD63. Objetivo: Padronizar e validar o BAT para ácido acetilsalicílico (AAS), diclofenaco, dipirona e paracetamol em pacientes com hipersensibilidade a AINEs. Metodologia: Participaram 20 (testados com os quatro AINEs) + 33 (testados somente com AAS) pacientes atendidos no Serviço de Imunologia Clínica e Alergia do HCFMUSP, que apresentaram manifestações cutâneas em até 24 horas após exposição a um ou múltiplos AINEs, bem como 13 (quatro AINEs) + 26 (AAS) controles. A técnica consistiu em incubar sangue total com os AINEs já mencionados e, depois, marcar as amostras com anticorpos monoclonais (CD45, anti-IgE e CD63) para posterior leitura por citometria de fluxo. Os resultados obtidos foram comparados com as histórias clínicas e os testes de provocação oral, quando realizados. Resultados: Utilizando os critérios de positividade do BAT empregados na literatura (isto é, porcentagem de CD45+IgE+highCD63+ e índice de estimulação), a sensibilidade e a especificidade variaram de acordo com o AINE: para ácido acetilsalicílico foram 75,0% e 16,7%, respectivamente, diclofenaco, 100% e 0%, dipirona, 23,5% e 66,7%, paracetamol, 40,0% e 42,9%. Após a realização de curvas dose-resposta e tempo-resposta somente com AAS, foi encontrado novo critério de positividade: média de intensidade de fluorescência (MFI) menor do que 6575 representava BAT positivo; com isso, os valores de sensibilidade e especificidade foram: 84,4% e 34,6%, respectivamente. O BAT foi mais sensível em pacientes cuja última reação ocorreu há menos de um ano da data de execução do BAT (93,7%). Conclusão: Devido aos baixos valores de sensibilidade e/ou especificidade, não foi possível padronizar e, por conseguinte, validar o BAT para ácido acetilsalicílico, diclofenaco, dipirona e paracetamol.
Introduction: Currently, the diagnosis of nonsteroidal antiinflammatory drugs (NSAIDs) hypersensivitity is based on patients´ clinical history and drug provocation tests, which are done in selected cases. Nevertheless, this test may expose patients to severe risks, including anaphylaxis. Looking for a safer tool, Basophil Activation Test (BAT) for allergy diagnosis has been studied in the last years. It is an in vitro method where a wide variety of stimuli can be tested, incubating them with the patient\'s blood sample, and observing basophil activation (indication of hypersensitivity) through upregulation of CD63 (or other basophil activation markers) on this leucocyte\'s membrane. Objective: To standardize and validate BAT stimulated with acetylsalicylic acid (ASA), diclophenac, dipyrone and paracetamol in NSAID hypersensitive patients. Methods: Patients which reported immediate reactions (less than 24 hours) after exposure to one or multiple NSAIDs, with cutaneous symptoms were enrolled from Clinical Immunology and Allergy outpatient clinic from HC-FMUSP. BAT with the four NSAIDs was tested on 20 patients and 13 controls and BAT with ASA only, on 33 patients and 26 controls. BAT consisted of incubating whole blood with NSAIDs, then triple-labeled with monoclonal antibodies (CD45, anti-IgE, CD63) for analysis by flow cytometry. BAT results were compared to clinical history and oral provocation tests, when available. Results: According to literature\'s positivity criteria (percentage of CD45+IgE+highCD63+ and stimulation index), sensitivity and specificity varied according to the NSAID tested: for ASA was 75.0% and 16.7% respectively, diclophenac, 100.0% and 0.0%, dipyrone, 23.5% and 66.7%, paracetamol, 40.0% and 42.9%. A new positivity criterion was possible to be defined after further dose-response and time-response curves only for ASA: Mean Fluorescence Intensity lower than 6575 (positive BAT). Accordingly, new sensitivity and specificity for BAT in ASA hypersensitivity were 84,4% and 34,6%. Patients that presented the last reaction in the last year were more likely to present a positive BAT (93.7%). Conclusion: Due to low values for sensitivity and/or specificity, it was not possible to standardize and validate BAT for ASA, diclophenac, dipyrone and paracetamol.
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Griveau, Audrey. "" Locked Nucleic Acid " nanovectorisés pour la répression de l'activité de microARN impliqués dans la radiorésistance des cellules de glioblastome." Phd thesis, Université d'Angers, 2013. http://tel.archives-ouvertes.fr/tel-01065649.

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Le glioblastome est la tumeur maligne primaire du cerveau la plus courante et la plus agressive chez l'homme. Son traitement conventionnel est palliatif et l'apparition de récidives est systématique. Dans le but de développer des thérapies innovantes basées sur le ciblage de nouvelles entités tumorales à l'aide de nanovecteur de médicaments, deux cibles ont été investiguées : le marqueur de radiorésistance AC133/1 et les onco-microARN. En utilisant des cellules de glioblastomes issues de patients, nous avons démontré que leur expansion in vitro à une pO2 non-physiologique (21%) altère leur agressivité tumorale in vivo et l'expression originelle d'AC133/1, au contraire d'une pO2 physiologique (3%) soulignant qu'AC133/1 est un marqueur précoce de non exposition à des pO2 élevées. Nous identifions par ailleurs un rôle pour AC133/1 dans l'endocytose du récepteur de la transferrine et son partenariat avec le métabolisme du fer. Enfin nous avons développé et caractérisé des immunonanoparticules capables de véhiculer des chimiothérapies ou des radiopharmaceutiques vers cet épitope fonctionnel. Dans un second axe de recherche, en parallèle d'établir le miRnome humain en réponse à l'action d'une radiothérapie, des nanocapsules lipidiques biomimétiques présentant à leur surface des peptides de papillomavirus et capables de se complexer avec des acides nucléiques antagonistes de microARN ont été développées et évaluées, démontrant leur intérêt en synergie d'une radiothérapie. Collectivement et en amont d'expérimentations in vivo en cours, ces résultats soulignent la pertinence d'appliquer de nouvelles nanomédecines ciblées pour le contournement de la radiorésistance dans le glioblastome.
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Books on the topic "Antigen CD163"

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name, No. Ectopeptidases: CD13/aminopeptidase N and CD26/dipeptidylpeptidase IV in medicine and biology. New York, NY: Kluwer Academic/Plenum, 2003.

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(Editor), Jürgen Langner, and Siegfried Ansorge (Editor), eds. Ectopeptidases: CD13/Aminopeptidase N and CD26/Dipeptidylpeptidase IV in Medicine and Biology. Springer, 2002.

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Book chapters on the topic "Antigen CD163"

1

Herold-Mende, Christel, and Benito Campos. "Glioma Patients: Role of CD133 Stem Cell Antigen." In Stem Cells and Cancer Stem Cells, Volume 1, 69–76. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1709-1_8.

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Joo, Kyeung Min, and Do-Hyun Nam. "Prospective Identification of Cancer Stem Cells with the Surface Antigen CD133." In Methods in Molecular Biology, 57–71. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-280-9_5.

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Kanzaki, Hideharu, Kimitoshi Imai, Hiroshi Fujiwara, Michiyuki Maeda, and Takahide Mori. "The Expression of Peptidase Antigens, CD10/Neutral Endopeptidase, CD13/Aminopeptidase N, and CD26/Dipeptidyl Peptidase IV in Human Endometrium." In Endocrinology of Embryo-Endometrium Interactions, 67–75. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1881-5_7.

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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD163." In The Leucocyte Antigen FactsBook, 427–28. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50564-3.

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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD103." In The Leucocyte Antigen FactsBook, 379–80. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50542-4.

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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD153." In The Leucocyte Antigen FactsBook, 417–18. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50560-6.

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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD161." In The Leucocyte Antigen FactsBook, 421–23. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50562-x.

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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD162." In The Leucocyte Antigen FactsBook, 424–26. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50563-1.

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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD166." In The Leucocyte Antigen FactsBook, 429–30. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50565-5.

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Barclay, A. Neil, Marion H. Brown, S. K. Alex Law, Andrew J. McKnight, Michael G. Tomlinson, and P. Anton van der Merwe. "CD13." In The Leucocyte Antigen FactsBook, 166–68. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012078185-0/50447-9.

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Conference papers on the topic "Antigen CD163"

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Vora, Parvez, Chitra Venugopal, Sujeivan Mahendram, Chirayu Chokshi, Maleeha Qazi, Minomi Subapanditha, Mohini Singh, et al. "Abstract 2300: Human CD133-specific chimeric antigen receptor (CAR) modified T cells target patient-derived glioblastoma brain tumors." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2300.

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Chen, Long, Vicky Li, David Allan, Robert Reger, Elena Cherkasova, Stephanie Pierre, Stefan Barisic, et al. "Abstract 1434: The Costimulatory Signal Domains 4-1BB and CD3ζ Do Not Improve the Function of CD16A Chimeric Antigen Receptor Transduced NK Cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1434.

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Chen, Long, Vicky Li, David Allan, Robert Reger, Elena Cherkasova, Stephanie Pierre, Stefan Barisic, et al. "Abstract 1434: The Costimulatory Signal Domains 4-1BB and CD3ζ Do Not Improve the Function of CD16A Chimeric Antigen Receptor Transduced NK Cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1434.

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LaFleur, David W., Haiying Qin, Justin P. Edwards, Liubov Zaritskaya, Ankit Gupta, C. Jenny Mu, Laura K. Richman, Terry J. Fry, and David M. Hilbert. "Abstract 601: Chimeric antigen receptors incorporating novel binding domains targeting CD123 direct potent antitumor activity of T cells: Correlation between affinity and activity." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-601.

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Zekri, Abdel-Rahman N., and Abeer Bahnassy. "Abstract 3540: Evaluation of Alpha-fetoprotein (AFP), telomerase, melanoma associated antigen (MAGE1 and MAGE 3), cancer stem cell markers cytokeratin (CK) and (CD133,) as potential biomarkers for hepatocellular carcinoma (HCC)." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3540.

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