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Letteratura scientifica selezionata sul tema "T cell"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 9 giugno 2025

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Articoli di riviste sul tema "T cell"

1

Ohshima, Kôichi, Junji Suzumiya, and Masahiro Kikuchi. "T cell rich B cell lymphoma." Journal of the Japan Society of the Reticuloendothelial System 36, no. 5-6 (1996): 391–93. http://dx.doi.org/10.3960/jslrt1961.36.391.

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2

Y, Elshimali. "Chimeric Antigen Receptor T-Cell Therapy (Car T-Cells) in Solid Tumors, Resistance and Success." Bioequivalence & Bioavailability International Journal 6, no. 1 (2022): 1–6. http://dx.doi.org/10.23880/beba-16000163.

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CARs are chimeric synthetic antigen receptors that can be introduced into an immune cell to retarget its cytotoxicity toward a specific tumor antigen. CAR T-cells immunotherapy demonstrated significant success in the management of hematologic malignancies. Nevertheless, limited studies are present regarding its efficacy in solid and refractory tumors. It is well known that the major concerns regarding this technique include the risk of relapse and the resistance of tumor cells, in addition to high expenses and limited affordability. Several factors play a crucial role in improving the efficacy of immunotherapy, including tumor mutation burden (TMB), microsatellite instability (MSI), loss of heterozygosity (LOH), the APOBEC Protein Family, tumor microenvironment (TMI), and epigenetics. In this minireview, we address the current and future applications of CAR T-Cells against solid tumors and their measure for factors of resistance and success.

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3

CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.

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4

Rimpo, Kenji, Yumiko Kagawa, and Tetsushi Yamagami. "T-cell-rich B-cell lymphoma in a dog." Journal of Japan Veterinary Cancer Society 4, no. 1 (2013): 1–5. http://dx.doi.org/10.12951/jvcs.2012-001.

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5

Toner, Keri, Catherine M. Bollard, and Hema Dave. "T-cell therapies for T-cell lymphoma." Cytotherapy 21, no. 9 (September 2019): 935–42. http://dx.doi.org/10.1016/j.jcyt.2019.04.058.

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6

Fitch, F. W. "T-cell clones and T-cell receptors." Microbiological Reviews 50, no. 1 (1986): 50–69. http://dx.doi.org/10.1128/mmbr.50.1.50-69.1986.

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Fitch, F. W. "T-cell clones and T-cell receptors." Microbiological Reviews 50, no. 1 (1986): 50–69. http://dx.doi.org/10.1128/mr.50.1.50-69.1986.

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8

Mohapatra, Manisha, and Yerraguntala Subramanya Sarma. "T-Cell/ Histiocyte-Rich Large B-Cell Lymphoma of Posterior Mediastinum." Annals of Pathology and Laboratory Medicine 6, no. 6 (June 24, 2019): C63–66. http://dx.doi.org/10.21276/apalm.2389.

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9

Chinnikatti, Shravana kumar, Soumya shravan, H. N. Asikur Rahaman, and Shraavya Shraavya. "New Treatments for Synovial Cell Sarcoma with Genetically Modified T-Cell?" Cancer Research and Cellular Therapeutics 6, no. 3 (May 16, 2022): 01–02. http://dx.doi.org/10.31579/2640-1053/113.

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Synovial cell sarcoma is rare but very aggressive tumour if not treated early, due to the painless nature of this tumour patients normally come in late and advances stage, can occur in bones, muscle cells, cartilages, ligaments and de-novo from pleuripotent stem cells from asnywhere in the body but most commonly arm, leg, or foot, and near joints such as the wrist or ankle and possibly from any joints in the body, even from soft tissues of lung and abdomen, the other name for this tumour is called malignant synovioma.The 5 year survival after the effective primary treatment is 30-75% and the survival rate is less than 5% if the tumour recurred within 1 year of primary treatment and that’s why new treatments are explored continuously. Due to late recognition and diagnosis of this rare tumour leads to many problems in treatment and in disease course. This tumour can occur at any age but is most common in growing periods like teen agers and adolescents. This tumour can spread to any organ in the body but most commonly distant metastases occur in lungs. Synovial sarcomas actually a misnomer as previously thought, now with advances in cell structure advances, These tumours can occur not only from synovial cells but from any cell of bone, muscle, tendon, ligaments and cartilage forming cells and supporting cells. These tumours occur with equal propensity in both men and women of younger age. If diagnosed early and treated early with surgery alone patients can be cured completely without any morbidity and mortality

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Udhayakumar, Venkatachalam, Bondada Subbarao, Aruna Seth, Mitzi Nagarkatti, and Prakash S. Nagarkatti. "Impaired autoreactive T cell-induced T cell-T cell interaction in aged mice." Cellular Immunology 116, no. 2 (October 1988): 299–307. http://dx.doi.org/10.1016/0008-8749(88)90232-8.

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Tesi sul tema "T cell"

1

Sarris, Milka. "Dynamics of helper T cell and regulatory T cell interactions with dendritic cells." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611896.

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2

Carson, Bryan David. "Impaired T cell receptor signaling in regulatory T cells /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8337.

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3

Lloyd, Angharad. "Gene editing in T-cells and T-cell targets." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/98512/.

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Recent years have witnessed a rapid proliferation of gene editing in mammalian cells due to the increasing ease and reduced cost of targeted gene knockout. There has been much excitement about the prospect of engineering T-cells by gene editing in order to provide these cells with optimal attributes prior to adoptive cell therapy for cancer and autoimmune disease. I began by attempting to compare short hairpin RNA (shRNA) and zinc finger nuclease (ZFN) approaches using the CD8A gene as a target for proof of concept of gene editing in Molt3 cells. During the course of my studies the clustered regularly interspaced short palindromic repeats (CRISPR) mechanism for gene editing was discovered so I also included CRISPR/Cas9 in my studies. A direct comparison of the three gene editing tools indicated that the CRISPR/Cas9 system was superior in terms of ease, efficiency of knockout and cost. As the use of gene editing tools increases there are concerns about the inherent risks associated with the use of nuclease based gene editing tools prior to cellular therapy. Expression of nucleases can lead to off target mutagenesis and malignancy. To circumvent this problem I generated a non-nuclease based gene silencing system using the CD8A zinc finger (ZF) fused to a Krüppel associated box (KRAB) repressor domain. The ZF-KRAB fusion resulted in effective silencing of the CD8A gene in both the Molt3 cell line and in primary CD8+ T-cells. Importantly, unlike CRISPR/Cas9 based gene editing, the ZF-KRAB fusion was small enough to be transferred in a single lentiviral vector with a TCR allowing simultaneous redirection of patient T-cell specificity and alteration of T-cell function in a single construct. To improve the efficiency of gene editing with CRISPR/Cas9 I developed an ‘all in one’ CRISPR/Cas9 system which incorporated all elements of the CRISPR/Cas9 gene editing system in a single plasmid. The ‘all in one’ system was utilised to derive MHC-related protein 1 (MR1) deficient clones from the A549 lung carcinoma and THP-1 monocytic cell lines in order to study MR1 biology. Mucosal-associated invariant T-cell (MAIT) clones were not activated by MR1 deficient A549 or THP-1 clones infected with bacteria.

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Stefkova, Martina. "Regulatory T cells control the CD4 T cell repertoire." Doctoral thesis, Universite Libre de Bruxelles, 2016. https://dipot.ulb.ac.be/dspace/bitstream/2013/233151/3/Table.pdf.

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Des études récentes menées chez l’homme et la souris ont suggéré que la diversité du répertoire TCR pourrait jouer un rôle dans la protection contre des pathogènes à haut pouvoir mutagène. Afin d’étudier le répertoire des lymphocytes T CD4, nous avons utilisé un modèle de souris TCRβ transgéniques exprimant une chaine β spécifique du peptide env122-141 dans le contexte du MHCII. Suite à l’immunisation des souris TCRβ transgéniques avec des cellules dendritiques pulsées avec le peptide env, une rapide prolifération et une restriction du répertoire des lymphocytes T Vα2 CD4 spécifiques est observée. L’analyse de la diversité du répertoire de ces cellules par séquençage à haut débit, a montré l’émergence d’un répertoire plus divers dans des souris déplétées en lymphocytes T régulateurs. Ces résultats suggèrent qu’en plus du rôle des Tregs dans le contrôle de la magnitude de la réponse immunitaire, ces cellules pourraient également contrôler la diversité du répertoire des lymphocytes T suite à une stimulation antigénique.<br>Recent studies conducted in mice and humans have suggested a role for the TCR repertoire diversity in immune protection against pathogens displaying high antigenic variability. To study the CD4 T cell repertoire, we used a mouse model in which T cells transgenically express the TCRβ chain of a TCR specific to a MHCII-restricted peptide, env122-141. Upon immunization with peptide-pulsed dendritic cells, antigen-specific Vα2+ CD4+ T cells rapidly expand and display a restricted TCRα repertoire. In particular, analysis of receptor diversity by high-throughput TCR sequencing in immunized mice suggests the emergence of a broader CDR3 Vα2 repertoire in Treg-depleted mice. These results suggest that Tregs may play a role in the restriction of the CD4 T cell repertoire during an immune response, raising therefore the possibility that in addition to controlling the magnitude of an immune response, regulatory cells may also control the diversity of TCRs in response to antigen stimulation.<br>Doctorat en Sciences<br>info:eu-repo/semantics/nonPublished

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5

Smith, Trevor Robert Frank. "Modulation of CD4+ T cell responses by CD4+CD25+ regulatory T cells and modified T cell epitopes." Thesis, Imperial College London, 2004. http://hdl.handle.net/10044/1/11317.

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6

Sommermeyer, Daniel. "Generation of dual T cell receptor (TCR) T cells by TCR gene transfer for adoptive T cell therapy." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16051.

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Die Herstellung von T-Zellen mit definierten Spezifitäten durch den Transfer von T-Zellrezeptor (TCR) Genen ist eine effiziente Methode, um Zellen für eine Immuntherapie bereitzustellen. Eine besondere Herausforderung ist dabei, ein ausreichend hohes Expressionsniveau des therapeutischen TCR zu erreichen. Da T-Zellen mit einem zusätzlichen TCR ausgestattet werden, entsteht eine Konkurrenzsituation zwischen dem therapeutischen und dem endogenen TCR. Bevor diese Arbeit begonnen wurde war nicht bekannt, welche TCR nach einem Gen-Transfer exprimiert werden. Daher haben wir Modelle etabliert, in denen TCR Gene in Maus und humane T-Zellen mit definierten endogenen TCR transferiert wurden. Die Expression beider TCR wurde mithilfe von Antikörpern und MHC-Multimeren analysiert. Diese Modelle haben gezeigt, dass bestimmte TCR andere TCR von der Zelloberfläche verdrängen können. Dies führte in einem Fall zu einer vollständigen Umkehr der Antigenspezifität. Aufgrund dieser Ergebnisse haben wir das Konzept von „starken“ (gut exprimierten) und „schwachen“ (schlecht exprimierten) TCR vorgeschlagen. Zusätzlich wurde die Verdrängung „schwacher“ und „starker“ humaner TCR durch Maus TCR beobachtet. Parallel dazu wurde berichtet, dass die konstanten (C) Regionen von Maus TCR für die erhöhte Expression auf humanen Zellen verantwortlich sind. Dies führte zu einer Strategie zur Verbesserung der Expression humaner TCR, die auf dem Austausch der humanen C-Regionen durch die von Maus TCR basiert (Murinisierung). Ein Problem ist dabei die mögliche Immunogenität dieser hybriden Konstrukte. Deshalb haben wir jene Bereiche der Maus C-Regionen identifiziert, die für die erhöhte Expression verantwortlich sind. In der TCRalpha Kette wurden vier und in der TCRbeta Kette fünf Aminosäuren gefunden, die ausreichend für diesen Effekt waren. Primäre humane T-Zellen mit TCR, die diese neun „Maus“ Aminosäuren enthielten, zeigten eine bessere Funktionalität als T-Zellen mit Wildtyp TCR.<br>The in vitro generation of T cells with a defined antigen specificity by T cell receptor (TCR) gene transfer is an efficient method to create cells for immunotherapy. One major challenge of this strategy is to achieve sufficiently high expression levels of the therapeutic TCR. As T cells expressing an endogenous TCR are equipped with an additional TCR, there is a competition between therapeutic and endogenous TCR. Before this work was started, it was not known which TCR is present on the cell surface after TCR gene transfer. Therefore, we transferred TCR genes into murine and human T cells and analyzed TCR expression of endogenous and transferred TCR by staining with antibodies and MHC-multimers. We found that some TCR have the capability to replace other TCR on the cell surface, which led to a complete conversion of antigen specificity in one model. Based on these findings we proposed the concept of ‘‘strong’’ (well expressed) and “weak” (poorly expressed) TCR. In addition, we found that a mouse TCR is able to replace both “weak” and “strong” human TCR on human cells. In parallel to this result, it was reported that the constant (C)-regions of mouse TCR were responsible for the improved expression of murine TCR on human cells. This led to a strategy to improve human TCR by exchanging the C-regions by their murine counterparts (murinization). However, a problem of these hybrid constructs is the probable immunogenicity. Therefore, we identified the specific parts of the mouse C-regions which are essential to improve human TCR. In the TCRalpha C-region four and in the TCRbeta C-region five amino acids were identified. Primary human T cells modified with TCR containing these nine “murine” amino acids showed an increased function compared to cells modified with wild type TCR. For TCR gene therapy the utilization of these new C-regions will reduce the amount of foreign sequences and thus the risk of immunogenicity of the therapeutic TCR.

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7

Tyznik, Aaron Jacob. "CD4+ T cell help for CD8+ T cell responses /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8314.

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8

Butcher, Sarah A. "T cell receptor genes of influenza A haemagglutinin specific T cells." Thesis, University College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315271.

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9

Raeiszadeh, Mohammad. "Reconstitution of CMV-specific T-cells following adoptive T-cell immunotherapy and haematopoietic stem cell transplantation." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6968/.

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This thesis investigated reconstitution of CMV-specific T-cells in two cohorts of HSCT patients and studied the potential role of Tumour Necrosis Factor Receptor 2 (TNFR2) in regulation of CMV-specific T-cell expansion post HSCT. The first cohort included patients of a randomized phase II trial of adoptive cellular therapy for CMV-specific CD8\(^+\) T-cells. Cellular therapy resulted in earlier and greater expansion of CMV-specific CD8\(^+\) T cells and also reconstitution of CMV-specific CD4\(^+\) and non-infused CMV-specific CD8\(^+\) T-cells. The number of infused therapeutic T-cells and circulating levels of Alemtuzumab were found to influence immunotherapy. Additionally, reconstitution of CMV-specific CD4\(^+\) T-cells was studied using HLA-class II tetramers. CMV-specific CD4\(^+\) T-cell count of >0.7x10\(^3\)/ml was found to protect from recurrent CMV reactivation. One third of specific CD4\(^+\) T-cells were perforin and granzyme-B positive indicating cytotoxic potential, whilst the majority expressed T-bet. Expression of CD57 molecule on CD4\(^+\) T-cells was demonstrated as a potential biomarker of immune response to CMV. Also, distinct cytokine receptor expression patterns in naïve versus memory T-cells were observed. The results showed rapid decrease in IL-6R and increase in expression of TNFR2 after T-cell differentiation from naïve to effector cells and engagement of TNFR2 led to the apoptosis of CMV-specific T-cells.

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Kanazawa, Nobuo. "Fractalkine and macrophage-derived chemokine : T cell attracting chemokines expressed in T cell area dendritic cells." Kyoto University, 2000. http://hdl.handle.net/2433/180886.

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Libri sul tema "T cell"

1

1956-, Zhang Jingwu, and Cohen Irun R, eds. T-cell vaccination. New York: Nova Biomedical Books, 2008.

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2

Kearse, Kelly P. T Cell Protocols. New Jersey: Humana Press, 1999. http://dx.doi.org/10.1385/1592596827.

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Lugli, Enrico, ed. T-Cell Differentiation. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6548-9.

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Rainger, George Edward, and Helen M. Mcgettrick, eds. T-Cell Trafficking. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6931-9.

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5

Foss, Francine, ed. T-Cell Lymphomas. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-170-7.

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6

Verma, Navin Kumar, ed. T-Cell Motility. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9036-8.

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Libero, Gennaro, ed. T Cell Protocols. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-527-9.

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Marelli-Berg, Federica M., and Sussan Nourshargh, eds. T-Cell Trafficking. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-461-6.

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Bosselut, Rémy, and Melanie S. Vacchio, eds. T-Cell Development. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5.

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Bosselut, Remy, and Melanie S. Vacchio, eds. T-Cell Development. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2740-2.

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Capitoli di libri sul tema "T cell"

1

Gooch, Jan W. "T Cell." In Encyclopedic Dictionary of Polymers, 927. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14928.

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2

Bland, P. W. "Mucosal T Cell-Epithelial Cell Interactions." In Mucosal T Cells, 40–63. Basel: KARGER, 1998. http://dx.doi.org/10.1159/000058714.

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3

Simmons, Amie, and José Alberola-Ila. "Retroviral Transduction of T Cells and T Cell Precursors." In T-Cell Development, 99–108. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_8.

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4

Chen, C. H., A. Six, T. Kubota, S. Tsuji, F. K. Kong, T. W. F. Göbel, and M. D. Cooper. "T Cell Receptors and T Cell Development." In Current Topics in Microbiology and Immunology, 37–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80057-3_5.

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Yamaguchi, Motoko, and Kensei Tobinai. "NK-Cell Neoplasms." In T-Cell Lymphomas, 87–103. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-170-7_6.

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Sarris, Milka, and Alexander G. Betz. "Live Imaging of Dendritic Cell–Treg Cell Interactions." In Regulatory T Cells, 83–101. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61737-979-6_7.

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Vacchio, Melanie S., Thomas Ciucci, and Rémy Bosselut. "200 Million Thymocytes and I: A Beginner’s Survival Guide to T Cell Development." In T-Cell Development, 3–21. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_1.

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Wohlfert, Elizabeth A., Andrea C. Carpenter, Yasmine Belkaid, and Rémy Bosselut. "In Vitro Analyses of T Cell Effector Differentiation." In T-Cell Development, 117–28. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_10.

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Ross, Jenny O., Heather J. Melichar, Joanna Halkias, and Ellen A. Robey. "Studying T Cell Development in Thymic Slices." In T-Cell Development, 131–40. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_11.

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Cunningham, Cody A., Emma Teixeiro, and Mark A. Daniels. "FTOC-Based Analysis of Negative Selection." In T-Cell Development, 141–49. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_12.

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Atti di convegni sul tema "T cell"

1

Mamonkin, Maksim. "Abstract IA17: CAR T cells for T-cell lymphoma." In Abstracts: AACR Virtual Meeting: Advances in Malignant Lymphoma; August 17-19, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2643-3249.lymphoma20-ia17.

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van der Stegen, Sjoukje J. C., Maria Themeli, Justin Eyquem, Jorge Mansilla-Soto, and Michel Sadelain. "Abstract 2309: T-cell development from T cell-derived induced pluripotent stem cell." 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.am2016-2309.

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3

Duan, Zhipu, Zhuohui Lin, and Shijie Zhou. "Universal CAR T cell: engineering of universal T cell, modular CAR system, and applications." In 2021 International Conference on Medical Imaging, Sanitation and Biological Pharmacy. Clausius Scientific Press, 2021. http://dx.doi.org/10.23977/misbp.2021036.

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Abstract (sommario):

Universal Chimeric Antigen Receptor T cells (CAR T), an alternative design based on conventional CAR T cells, uses a switchable adaptor for a better redirection towards the target site. This technology overcomes the obstacles of the conventional Car T cells system, such as immunogenicity, massive expression of cytokine and fixed antigen specificity. This article introduces universal CAR T cells from both the perspectives of the universal T cells and its modular CAR systems, illustrating the advancement of universal CAR T cells to overcome the limitation of conventional CAR T cells and serve as a more controllable and highly promising system. The universal CAR T cells section focuses on the challenges of choosing T cell sources and the corresponding solutions, while the modular CAR system section summarizes the different types of switchable adaptors in combination with clinical applications in various types of cancer treatments. Overall, universal CAR T cells therapy is a novel development that not only out-competes but also recovers the shortage of the conventional CAR T cells system. With the use of switchable adaptors, the universal CAR T cells system is commercially beneficial for the public and a safe product to allow the industry to expand the clinical application of different types of cancers.

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Jakobsen, Bent. "Abstract 2802: Fine-tuning T cell receptors for adoptive T cell therapy." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2802.

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Wilking, Alice, Lili Wang, Benjamin K. Chen, Thomas Huser, and Wolfgang Hubner. "Resolving T cell — T cell transfer of HIV-1 by optical nanoscopy." In 2017 Conference on Lasers and Electro-Optics Europe (CLEO/Europe) & European Quantum Electronics Conference (EQEC). IEEE, 2017. http://dx.doi.org/10.1109/cleoe-eqec.2017.8087773.

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6

Kristensen, Nikolaj Pagh, Christina Heeke, Siri A. Tvingsholm, Anne-Mette Bjerregaard, Arianna Draghi, Amalie Kai Bentzen, Rikke Andersen, Marco Donia, Inge Marie Svane, and Sine Reker Hadrup. "Abstract A14: Neoepitope-specific CD8+ T cells in adoptive T-cell transfer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a14.

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7

Chen, Gregory M., Changya Chen, Rajat K. Das, Yang-Yang Ding, Bing He, Hannah Kim, David M. Barrett, and Kai Tan. "Abstract 4236: A subtype-specific T-cell transcriptomic atlas reveals determinants of T-cell dysfunction in CAR T-cell therapy resistance." 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.am2020-4236.

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8

Ho, Chen-Ta, and Cheng-Hsien Liu. "Micro T-Switches for Cell Sorting Applications." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61427.

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Abstract (sommario):

A new micro-T-switch actuated by electrochemical bubbles for cells sorting has been proposed and successfully demonstrated by MEMS micromachining technique. We take advantage of electrolysis-bubbles, which have the features of low operation temperature and high surface-tension force, to actuate the micro T- switches in our device. The micro-T-switch is placed at the junction of the T-shapes microchannel. The movable T-structure design makes cell sorting active and programmable compared with other passive cell sorting mechanism such as micro-filters. Furthermore, the low operation temperature for electrolysis - bubbles driving mechanism could minimize cell-damage that happens in conventional high electric-separation instruments, such as Flow Cytometry.

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Eun, So-Young. "Abstract 1645: CEACAM1-blockade for T-cell activation and antitumor T-cell response." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1645.

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Takahashi, Hideyuki, Paulina Pathria, Ryan Shepard, Ann Shih, Tiani L. Louis та Judith A. Varner. "Abstract A86: PI3Kγ inhibition activates T cell memory and relieves T cell exhaustion". У Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a86.

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Rapporti di organizzazioni sul tema "T cell"

1

HLADEK, K. L. T Plant Cell Investigation. Office of Scientific and Technical Information (OSTI), September 2001. http://dx.doi.org/10.2172/807319.

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2

Bonnett, Megan. CAR T Cell Therapy. Ames (Iowa): Iowa State University, January 2019. http://dx.doi.org/10.31274/cc-20240624-337.

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3

Yompakdee, Chulee, and Sittiruk Roytrakul. Molecular target of an anti-cancer compound from leaves of Clausena harmandiana (Pierre). Chulalongkorn University, 2016. https://doi.org/10.58837/chula.res.2016.32.

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Abstract (sommario):

Clausena harmandiana (Pierre) Guillaumin or Song faa dong (in Thai), is classified in Family Rutaceae. Previous study, a coumarin compound designated CHA-01 was isolated from leave extract of C. harmandiana with inhibitory activity against calcium signaling in a ZDS1 null mutant yeast Saccharomyces cerevisiae (delta zds1). However, not much has been known on biological activity of this coumarin. In the past, some other coumarins were reported to contain anti-cancer activity. The aim of this research was to study molecular mechanism on antiproliferation activity of CHA-01 in Jurkat T cells. The results revealed that CHA-01 showed anti-proliferative activity in several cell lines including Jurkat (Lymphocytic leukemic cell line), KATO III (Stomach cancer cell line) and THP1 (Monocytic leukemic cell line) by MTT assay. Jurkat T cell line was the most sensitity cell line to CHA-01 treatment with IC50 value of 0.67 μM. It contained no cytotoxic activity against normal lymphocytes up to 10 μM. Flow cytometric analysis revealed that the CHA-01 caused cell cycle arrest at S phase in Jurkat T cells as a result from inhibition of DNA synthesis. Moreover, CHA-01 induced apoptotic cell death in the Jurkat T cells. Our results revealed the role(s) of CHA-01 on its anti-cancer activity especially against lymphocytic leukemia. Future study will utilize proteomic analysis on expression level of proteins in CHA-01 treated Jurkat T cells.

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4

Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada610046.

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5

Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada612327.

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6

Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada594698.

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7

Dotti, Gianpietro. Improve T Cell Therapy in Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada550874.

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8

Medof, M. E. Augmentation of Antitumor T-Cell Responses by Increasing APC T-Cell C5a/C3a-C5aR/C3aR Interactions. Fort Belvoir, VA: Defense Technical Information Center, March 2013. http://dx.doi.org/10.21236/ada585489.

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9

หังสสูต, ปกรัฐ, та ญาดา ตันสิริ. การวิเคราะห์การยับยั้งการเพิ่มจำนวนของไวรัสเอชไอวีโดยทีเซลล์ : การทดสอบที่ใช้วิเคราะห์ภูมิคุ้มกันที่ได้จากการกระตุ้นด้วยวัคซีนป้องกัน HIV : รายงานการวิจัย. คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2013. https://doi.org/10.58837/chula.res.2013.14.

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Introduction and Objective: Among HIV infected donors, the natural history of HIV infection is different and HIV load is the one of factors resulting in the different clinical outcome. We have been characterized HIV infected donors into 2 groups: controllers (HIV loads< 2,000 copies/ml) and noncontrollers (HIV loads > 2,000 copies/ml). In our previous study, we found that controllers who naturally control HIV infection have the higher number of HIV-gag p24 specific T cells than noncontrollers significantly. Thus, we hypothesized that these polyfunctional T cells can effectively suppress HIV replication leading to the low level of HIV loads in controllers. 3 Methods: The functional quality of T cells was detected using intracellular cytokine staining assay. HIV isolates were isolated from HIV infected donors and then superinfected with autologous CD4+ T cells. The different functional quality of HIV-gag p24 specific T cell lines and bulk CDS+ T cells were used as effectors in their autologous HIV suppression assay. HIV suppression was assessed using HIV-gag p24 ELISA assay. Results: In our study, controllers were significantly higher in the absolute number of full 5 functions, HIV-gag p24 specific T cells than noncontrollers. Moreover, in vitro HIV suppression assay has been shown that bulk CDS+ T cells from controllers can significantly suppress HIV replication when compared with noncontrollers. And, the HIV-gag p24 specific T cell line from controllers has the ability to suppress HIV replication in in vitro assay, effectively. Conclusion: HIV-gag p24 specific T cell responses from controllers have the superior effect on the suppression of HIV replication in vitro study.

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10

หังสสูต, ปกรัฐ, та ญาดา ตันสิริ. การวิเคราะห์การยับยั้งการเพิ่มจำนวนของไวรัสเอชไอวีโดยทีเซลล์ : การทดสอบที่ใช้วิเคราะห์ภูมิคุ้มกันที่ได้จากการกระตุ้นด้วยวัคซีนป้องกัน HIV : รายงานการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2014. https://doi.org/10.58837/chula.res.2014.19.

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Abstract (sommario):

Introduction and Objective: Among HIV infected donors, the natural history of HIV infection is different and HIV load is the one of factors resulting in the different clinical outcome. We have been characterized HIV infected donors into 2 groups: controllers (HIV loads <2,000 copies/ml) and noncontrollers (HIV loads >2,000 copies/ml).In our previous study, we founded that controllers who naturally control HIV infection have the higher number of HIV-gag p24 specific T cells than noncontrollers significantly. Thus, We hypothesized that these polyfunctional T cells can effectively suppress HIV replication leading to the low level of HIV loads in controllers. Methods: The functional quality of T cells was detected using intracellular cytokine staining assay. HIV isolates were isolated from HIV infected donors and then superinfected with autologous CD4+ T cells. The different functional quality of HIV-gag p24 specific T cell lines and bulk CD8+ T cells were used as effectors in their autologous HIV suppression assay. HIV suppression was assessed using HIV-gag p24 ELISA assay. Results: In our study, controllers were significantly higher in the absolute number of full 5 functions, HIV-gag p24 specific T cells than noncontrollers. Moreover, in vitro HIV suppression assay has been shown that bulk CD8+ T cells from controllers can significantly suppress HIV replication when compared with noncontrollers. And, the HIV-gag p24 specific T cell line from controllers has the ability to suppress HIV replication in in vitro assay, effectively. Conclusion: HIV-gag p24 specific T cell responses from controllers have the superior effect on the suppression of HIV replication in vitro study.

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