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Relevant bibliographies by topics / T-cell receptor

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Academic literature on the topic 'T-cell receptor'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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Journal articles on the topic "T-cell receptor"

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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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Robbins, Paul F. "T-Cell Receptor–Transduced T Cells." Cancer Journal 21, no. 6 (2015): 480–85. http://dx.doi.org/10.1097/ppo.0000000000000160.

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Sowka, Slawomir, Roswitha Friedl-Hajek, Ute Siemann, Christof Ebner, Otto Scheiner, and Heimo Breiteneder. "T Cell Receptor CDR3 Sequences and Recombinant T Cell Receptors." International Archives of Allergy and Immunology 113, no. 1-3 (1997): 170–72. http://dx.doi.org/10.1159/000237537.

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Akatsuka, Yoshiki. "IV. T-cell Receptor-engineered T Cells." Nihon Naika Gakkai Zasshi 108, no. 7 (July 10, 2019): 1384–90. http://dx.doi.org/10.2169/naika.108.1384.

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OMOTO, K., Y. Y. KONG, K. NOMOTO, M. UMESUE, Y. MURAKAMI, M. ETO, and K. NOMOTO. "Sensitization of T-cell receptor-αβ+ T cells recovered from long-term T-cell receptor downmodulation." Immunology 88, no. 2 (June 1996): 230–37. http://dx.doi.org/10.1111/j.1365-2567.1996.tb00009.x.

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Kamiya, Takahiro, Desmond Wong, Yi Tian Png, and Dario Campana. "A novel method to generate T-cell receptor–deficient chimeric antigen receptor T cells." Blood Advances 2, no. 5 (March 5, 2018): 517–28. http://dx.doi.org/10.1182/bloodadvances.2017012823.

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Key Points Newly designed PEBLs prevent surface expression of T-cell receptor in T cells without affecting their function. Combined with chimeric antigen receptors, PEBLs can rapidly generate powerful antileukemic T cells without alloreactivity.

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Sommermeyer, Daniel, Julia Neudorfer, Monika Weinhold, Matthias Leisegang, Boris Engels, Elfriede Noessner, Mirjam H M. Heemskerk, et al. "Designer T cells by T cell receptor replacement." European Journal of Immunology 36, no. 11 (November 2006): 3052–59. http://dx.doi.org/10.1002/eji.200636539.

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Rosenberg, Kenneth M., and Nevil J. Singh. "Subset-specific neurotransmitter receptor expression tunes T cell activation." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 47.22. http://dx.doi.org/10.4049/jimmunol.200.supp.47.22.

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Abstract T cells continually patrol and invade other tissues and are exposed to varying tissue-specific cues. Different tissues are typically innervated by neurons using characteristic neurotransmitters. Therefore, encounter with particular neurotransmitters has the potential to influence the tissue-specific behavior of T cells. Although neurons utilize a complex array of over 180 neurotransmitter receptor (NR) genes, we find that murine T cells in total express only a limited set (26 detected) of them. Furthermore, the expression is T cell subset-specific suggesting distinct functional roles. Several receptors, including Adrb2, Gabrr2, and Chrnb2, are most highly expressed in naïve CD4 T cells while CD8 T cells specifically express the glutamate receptor Gria3 and have high expression of the cannabinoid receptor Cnr2. Within the CD4 population, memory T cells upregulate Hrh4 and P2ry1 while the VIP receptor Vipr1 is uniquely absent from regulatory T cells. In order to understand how these distinct patterns affect immune responses, we are analyzing the functional impact of signaling T cells through them. Importantly, NR signaling pathways considerably overlap with T cell receptor (TCR) signaling pathways. Accordingly, preliminary data shows that a competing signal from NR receptors such as the β2 adrenergic, histamine H2, and VPAC1 (VIP) receptors dampens direct T cell activation through the CD3 complex. Determining how T cells integrate the complex contextual information they encounter in vivo guides our understanding of T cell decision making and will allow for the development of more targeted therapeutics.

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Lin, Joseph, and Arthur Weiss. "T cell receptor signalling." Journal of Cell Science 114, no. 2 (January 15, 2001): 243–44. http://dx.doi.org/10.1242/jcs.114.2.243.

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Ray, L. Bryan. "T cell receptor dynamics." Science 373, no. 6550 (July 1, 2021): 71.4–72. http://dx.doi.org/10.1126/science.373.6550.71-d.

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Dissertations / Theses on the topic "T-cell receptor"

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Soper, David Michael. "Interleukin-2 receptor and T cell receptor signaling in regulatory T cells /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8344.

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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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Im, Jin Seon. "Molecular characterization of T cell receptors and non-MHC restricted T cell receptor binding peptides." Diss., The University of Arizona, 1999. http://hdl.handle.net/10150/284969.

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T cells recognize antigenic peptides presented by MHC molecules on antigen presenting cells (APC) through T cell receptors (TCRs). Since TCRs are very similar to antibodies in structure and genetics, TCRs might have the potential to bind free antigens as antibodies do. Here, peptides which bound TCRs irrespective of MHC molecules have been identified by screening "one-bead one-peptide" combinatorial libraries. Peptides: VRENAR, RTGNYV, GKMHFK, KDAVKR and RKPQAI bound recombinant Jurkat single chain T cell receptors (scTcrs). GKMHFK, KDAVKR and RKPQAI were also specific for natural TCRs on the Jurkat cell surface. Molecular modeling implies that Glu96 in the CDR3 loop of TCR alpha chain is a candidate for the peptide interaction site. However, TCR-binding peptides did not induce biological effects on parental Jurkat cells. To extend this study to a biologically relevant system, diabetogenic T cells involved in insulin-dependent diabetes mellitus (IDDM) have been characterized. GAD(524-543) responding T cells showed restricted TCR variable gene usage, which utilized preferentially Vα17 and Vβ12. Three domain single chain T cell receptors (3D scTcr) were constructed as tools to investigate potential therapies for IDDM and to identify peptides which bind to TCR without association of MHC molecules. Functional analysis has demonstrated that GAD(524-543)-specific scTcrs retained the ability to bind GAD(524-543)/IAg7 complex. This work shows that recombinant scTcrs can bind cognate peptide presented by MHC molecules, therefore they can be used as substitutes for natural TCRs in screening "one-bead one-peptide" combinatorial libraries to identify TCR-binding peptide.

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Jiang, Ning. "Kinetic analysis of Fcγ receptor and T cell receptor interacting with respective ligands." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/26716.

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Low affinity Fcg receptor III (FcgRIII, CD16) triggers a variety of cellular events upon binding to the Fc portion of IgG. A real-time flow cytometry method was developed to measure the affinity and kinetics of such low affinity receptor/ligand interactions, which was shown as an easily operated yet powerful tool. Results revealed an unusual temperature dependence of reverse rate of CD16aTM dissociating from IgG. Except for a few studies using mammalian cell CD16s, most kinetics analyses use purified aglycosylated extracellular portion of the molecules, making it impossible to assess the importance of the receptor anchor and glycosylation on ligand binding. We used a micropipette adhesion frequency assay to demonstrate that the anchor length affects the forward rate and affinity of CD16s for IgG in a species specific manner, most likely through conformational changes. Receptor glycosylation dramatically reduced ligand binding by 100 folds. T cell receptor (TCR) is arguably the most important receptor in the adaptive human immune system. Together with coreceptor CD4 or CD8, TCR can discriminate different antigen peptides complexed with major histocompatibility complex (MHC) molecule (pMHC), which differ by as few as only one amino acid, and trigger different T cell responses. When T cell signaling was suppressed, TCR had similar affinity and kinetics for agonist and antagonist pMHC whose binding to CD8 was undetectable. TCR on activated T cell had a higher affinity for pMHCs, suggesting that TCRs organize themselves differently on activated T cells than on naïve T cells. In the absence of inhibitors for signaling, TCR binds agonist pMHC with several orders of magnitude higher affinity than antagonist pMHC. In addition, engagement of TCR by pMHC signals an upregulation of CD8 binding to pMHC, which is much stronger than the TCR-pMHC binding. The transition from weak TCR binding to the strong CD8 binding takes place around 0.75 second after TCR in contact with pMHC and can be reduced by several inhibitors of tyrosine and lipid phosphorylation, membrane rafts, and actin cytoskeleton. These results provide new insights to understanding T cell discrimination.

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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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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.
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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Li, Xiaoying. "T cell receptor repertoires of immunodominant CD8 T cell responses to Theileria parva." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/19552.

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Previous research has provided evidence that CD8 T cells mediate immunity against infection with Theileria parva. However, the immunity induced by one parasite strain doesn‟t give complete protection against other strains and this is associated with parasite strain specificity of the CD8 T cell responses. There is evidence that such strain specificity is a consequence of the CD8 T cell responses of individual animals being focused on a limited number of immunodominant polymorphic peptide-MHC determinants. Dominant responses to the Tp2 antigen have been demonstrated in animals homozygous for the A10 MHC haplotype. Three Tp2 epitopes recognised by A10+ animals (Tp249-59, Tp250-59 and Tp298-106) have been defined. This project set out to investigate the dominance of these epitopes and to examine the T cell receptor (TCR) repertoires of the responding T cells. The specific objectives were to: (i) Determine the dominance hierarchies of the three defined Tp2 epitopes in both A10-homozygous and -heterozygous cattle. (ii) Examine the clonal repertoires of epitope-specific responses by analysis of TCR gene expression. (iii) Isolate full-length cDNAs encoding TCR α and β chain pairs from T cell clones of defined epitope specificity and use them to generate cells expressing the functional TCRs. Using MHC class I tetramers the relative dominance of CD8 T cell responses were found to differ between A10-homozygous and heterozygous cattle. All A10-homozygous cattle examined had detectable responses to all 3 Tp2 epitopes, the Tp249-59 epitope consistently being the most dominant. By contrast, only some A10-heterozygous cattle had detectable responses to Tp2 and when present the response was specific only for the Tp298-106 epitope. Analyses of the sequences of expressed TCR β chains showed that the responses in individual animals were clonotypically diverse, but often contained a few large expanded clonotypes. The TCRs of Tp298-106–specific T cells showed preferential usage of the Vβ13.5 gene and the frequent presence of a “LGG” motif within the CDR3 of the B chain. A conserved (public) TCRβ clonotype shared by the Tp250-59-specific CD8 T cells from all A10-homozygous cattle was identified. The TCRα chains co-expressed with this public TCRβ clonotype were identified for a number of T cell clones. Lentivirus transduction of Jurkat cells with three full-length TCR α and β chain pairs resulted in successful expression of one of the α/β chain pairs as a functional TCR, thus providing the basis for future work to generate bovine T cells expressing defined TCRs in vitro.

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Wright, G. P. "Generation of antigen-specific regulatory T cells by T cell receptor gene transfer." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/18952/.

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Regulatory T cells (Tregs) have shown considerable potential in the treatment of murine models of immuno-pathology. Whilst poly-clonal Tregs are able to suppress immuno-pathology in a number of models, the superiority of Ag-specific Treg treatment has been demonstrated using Tregs from T cell receptor (TCR)- transgenic animals. Translation of these promising results to the clinic has been hampered by difficulties in isolating or enriching the rare Ag-specific Tregs from the polyclonal population. Here I describe two distinct approaches to generate Ag-specific T cells with regulatory ability: firstly, TCR gene transfer into purified CD4+CD25+ T cells was used to redirect the specificity of naturally occurring Tregs. Secondly, co-transfer of FoxP3 and TCR genes served to convert conventional CD4+ T cells into Ag-specific ‘Treg-like’ cells. Both approaches generated T cells that suppressed in vitro and engrafted efficiently, retaining TCR and FoxP3 expression, when adoptively transferred into recipient mice. Using an established arthritis model, I demonstrate Ag-driven accumulation of the gene modified T cells at the site of joint inflammation, which resulted in a reduction of joint swelling. In animals treated with TCR-transferred natural Tregs this was accompanied by a local reduction in the number of inflammatory Th17 cells and a significant decrease in arthritic bone destruction. Together, I have described a strategy to rapidly generate Ag-specific Tregs capable of antigen-dependent amelioration of autoimmune damage in the absence of general immune suppression. These approaches could practicably be translated into the clinic in order to treat numerous different immuno-pathologies.

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Moody, Anne Marie. "T-cell receptor studies in myasthenia gravis." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337448.

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Palmer, M. S. "Studies on the murine T-cell receptor." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379915.

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Books on the topic "T-cell receptor"

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Liu, Chaohong, ed. T-Cell Receptor Signaling. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0266-9.

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Henwood, Judith Ann. T-cell receptor expression in antigen-specific human T-cell clones. Birmingham: University of Birmingham, 1993.

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M, Davis Mark, and Buxbaum Joel, eds. T-cell receptor use in human autoimmune diseases. New York, N.Y: New York Academy of Sciences, 1995.

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Van den Elsen, Peter J., 1951-. The human T-cell receptor repertoire and transplantation. New York: Springer Verlag, 1995.

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R, Oksenberg Jorge, ed. The antigen T cell receptor: Selected protocols and applications. New York: R.G. Landes, 1997.

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van den Elsen, Peter J. The Human T-Cell Receptor Repertoire and Transplantation. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22494-6.

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Farhan, Ayar Jawi. T cell receptor gene polymorphism and usage in rheumatoid arthritis. Manchester: University of Manchester, 1997.

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M, Davis Mark, Kappler John, University of California, Los Angeles., and UCLA Symposium on the T Cell Receptor (1987 : Keystone, Colo.), eds. The T-cell receptor: Proceedings of a Smith Kline & French-UCLA symposium, held in Keystone, Colorado, April 26-May 1, 1987. New York: A.R. Liss, 1988.

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Afshari, Jalil Tavakol. Analysis of T cell antigen receptor [beta]-chain gene repertoires in alloreactive T lymphocytes. Manchester: University of Manchester, 1996.

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Oksenberg, Jorge R. Polymerase chain reaction and the analysis of the t cell receptor repertoire. Austin, Tex: R.G. Landes, 1992.

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Book chapters on the topic "T-cell receptor"

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Rojo, Jose M., Raquel Bello, and Pilar Portolés. "T-Cell Receptor." In Advances in Experimental Medicine and Biology, 1–11. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-09789-3_1.

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Loh, Dennis Y., Mark A. Behlke, and Hubert S. Chou. "T-Cell Receptor Genes." In The T-Cell Receptors, 89–99. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5406-2_4.

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Marrack, Phillipa, Kathryn Haskins, Neal Roehm, Janice White, Willi Born, Jordi Yagüe, Edward Palmer, and John W. Kappler. "The T-Cell Receptor." In Investigation and Exploitation of Antibody Combining Sites, 267–74. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5006-4_30.

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Ceri, Howard, and Chris Mody. "The T-Cell Receptor." In Immunology, Infection, and Immunity, 297–313. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555816148.ch13.

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Haskins, Kathryn, Neal Roehm, Charles Hannum, Janice White, Ralph Kubo, Philippa Marrack, and John Kappler. "The Murine T Cell Receptor." In Human T Cell Clones, 15–23. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4998-6_2.

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Sam-Yellowe, Tobili Y. "T Cell Development and T Cell Receptor Structure." In Immunology: Overview and Laboratory Manual, 105–16. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64686-8_13.

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Rioufol, Catherine, and Christian Wichmann. "Receiving, Handling, Storage, Thawing, Distribution, and Administration of CAR-T Cells Shipped from the Manufacturing Facility." In The EBMT/EHA CAR-T Cell Handbook, 37–43. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_7.

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Caccia, Nicolette, Rosanne Spolski, and Tak W. Mak. "Thymic Ontogeny and the T-Cell Receptor Genes." In The T-Cell Receptors, 101–15. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5406-2_5.

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Caccia, Nicolette, Barry Toyonaga, Nobuhiro Kimura, and Tak W. Mak. "The α and β Chains of the T-Cell Receptor." In The T-Cell Receptors, 9–51. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5406-2_2.

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Kirsch, Ilan R., and Gregory F. Hollis. "The Involvement of the T-Cell Receptor in Chromosomal Aberrations." In The T-Cell Receptors, 175–94. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5406-2_9.

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Conference papers on the topic "T-cell receptor"

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de Rooij, MAJ, DM Steen, D. Remst, A. Wouters, MGD Kester, RS Hagedoorn, PA van Veelen, EME Verdegaal, JHF Falkenburg, and MHM Heemskerk. "10.04 A library of novel cancer testis specific T-cell receptors for T-cell receptor gene therapy." In iTOC8 – the 8th Leading International Cancer Immunotherapy Conference in Europe, 8–9 October 2021, Virtual Conference. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jitc-2021-itoc8.4.

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Zijia, Cheng. "Chimeric-antigen Receptor T (CAR-T) Cell Therapy for Leukemia." In ICBET 2020: 2020 10th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3397391.3397451.

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Davis, Nicholas S., Catherine Leites, Helicia Paz, Leslie Ryan, Nathaniel Magilnick, Christian Hinrichs, Gang Zeng, and Erika von Euw. "Abstract 1496: KK-LC-1 targeting T cell receptor for adoptive T cell therapy." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1496.

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Sherwood, Anna M., Harlan Robins, Jonathan R. Fromm, Harvey A. Greisman, Daniel E. Sabath, Ryan O. Emerson, Mark Rieder, Brent Wood, and David Wu. "Abstract 1895: Identifying clonal T-cell receptor sequences and monitoring recurrent/persistent disease by T-cell receptor repertoire profiling in patients with mature T-cell neoplasms." 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.am2014-1895.

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Wu, Ling, Joanna Brzostek, Shvetha Sankaran, Triscilla Tan, Conrad Chan, Jiawei Yap, Junyun Lai, Paul MacAry, and Nicholas Gascoigne. "Abstract 1425: Chimeric antigen receptors based on T cell receptor-like antibodies." 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.sabcs18-1425.

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Wu, Ling, Joanna Brzostek, Shvetha Sankaran, Triscilla Tan, Conrad Chan, Jiawei Yap, Junyun Lai, Paul MacAry, and Nicholas Gascoigne. "Abstract 1425: Chimeric antigen receptors based on T cell receptor-like antibodies." 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.am2019-1425.

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Luo, Danhua. "Chimeric Antigen Receptor T-Cell Immunotherapy for Cancer." In BIBE2020: The Fourth International Conference on Biological Information and Biomedical Engineering. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3403782.3403802.

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Donaghey, Julie, Philippe Kieffer-Kwon, Troy Patterson, Tiffany Chan, Holly Horton, Robert Tighe, Dario A. Gutierrez, Daniel Getts, and Robert Hofmeister. "Abstract 2190: Engineering off-the-shelf T cell receptor fusion construct (TRuC) T cells." 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.am2020-2190.

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Donaghey, Julie, Philippe Kieffer-Kwon, Julio Gomez-Rodriguez, Troy Patterson, Jessica Gierut, Tiffany Chan, Ryan Milione, et al. "Abstract 1514: Engineering off-the-shelf T Cell Receptor Fusion Construct (TRuC) T cells." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1514.

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Matsuda, Tatsuo, Taigo Kato, Yuji Ikeda, Matthias Leisegang, Sachiko Yoshimura, Tetsuro Hikichi, Makiko Harada, et al. "Abstract 625: Eradication of cancer cells by T-cell receptor-engineered T cells targeting neoantigens/oncoantigens." 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.am2017-625.

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Reports on the topic "T-cell receptor"

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Weinberg, Andrew D. Tumor Specific CD4+ T-Cell Costimulation Through a Novel Receptor/Ligand Interaction. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada374764.

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Wiley, Don C., and David N. Garboczi. Structural Analysis of the Human T-Cell Receptor/HLA-A2/Peptide Complex. Fort Belvoir, VA: Defense Technical Information Center, August 1997. http://dx.doi.org/10.21236/ada342257.

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Weinberg, Andrew D. Tumor Specific CD4+ T-Cell Costimulation Through a Novel Receptor Ligand Interaction. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/ada359629.

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Gray, Andrew. Enhancing the Efficacy of Prostate Cancer Immunotherapy by Manipulating T-Cell Receptor Signaling in Order to Alter Peripheral Regulatory T-Cell Activity. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada511997.

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Gray, Andrew. Enhancing the Efficacy of Prostate Cancer Immunotherapy by Manipulating T-Cell Receptor Signaling in Order to Alter Peripheral Regulatory T-Cell Activity. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada553485.

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Zhao, Kangjia, Jiwen Sun, Nanping Shen, Mengxue He, Haishan Ruan, Geng Lin, Jiali Ma, and Yanhua Xu. Treatment-Related Adverse Events of Chimeric Antigen receptor T-Cell (CAR-T) Cell Therapy in B-cell hematological malignancies in the Pediatric and Young Adult Population: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0034.

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Bickel, Ulrich. Simultaneous Vascular Targeting and Tumor Targeting of Cerebral Breast Cancer Metastases Using a T-Cell Receptor Mimic Antibody. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada608026.

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Bickel, Ulrich. Simultaneous Vascular Targeting and Tumor Targeting of Cerebral Breast Cancer Metastases Using a T-Cell Receptor Mimic Antibody. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada586024.

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Zhu, Jun, Yuqin Song, and Zhitao Ying. Efficacy and safety of anti-CD19 chimeric antigen receptor-T cells immunotherapy in patients with relapsed or refractory large B-cell lymphoma: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0045.

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Altstein, Miriam, and Ronald J. Nachman. Rational Design of Insect Control Agent Prototypes Based on Pyrokinin/PBAN Neuropeptide Antagonists. United States Department of Agriculture, August 2013. http://dx.doi.org/10.32747/2013.7593398.bard.

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Abstract:

The general objective of this study was to develop rationally designed mimetic antagonists (and agonists) of the PK/PBAN Np class with enhanced bio-stability and bioavailability as prototypes for effective and environmentally friendly pest insect management agents. The PK/PBAN family is a multifunctional group of Nps that mediates key functions in insects (sex pheromone biosynthesis, cuticular melanization, myotropic activity, diapause and pupal development) and is, therefore, of high scientific and applied interest. The objectives of the current study were: (i) to identify an antagonist biophores (ii) to develop an arsenal of amphiphilic topically active PK/PBAN antagonists with an array of different time-release profiles based on the previously developed prototype analog; (iii) to develop rationally designed non-peptide SMLs based on the antagonist biophore determined in (i) and evaluate them in cloned receptor microplate binding assays and by pheromonotropic, melanotropic and pupariation in vivo assays. (iv) to clone PK/PBAN receptors (PK/PBAN-Rs) for further understanding of receptor-ligand interactions; (v) to develop microplate binding assays for screening the above SMLs. In the course of the granting period A series of amphiphilic PK/PBAN analogs based on a linear lead antagonist from the previous BARD grant was synthesized that incorporated a diverse array of hydrophobic groups (HR-Suc-A[dF]PRLa). Others were synthesized via the attachment of polyethylene glycol (PEG) polymers. A hydrophobic, biostablePK/PBAN/DH analog DH-2Abf-K prevented the onset of the protective state of diapause in H. zea pupae [EC50=7 pmol/larva] following injection into the preceding larval stage. It effectively induces the crop pest to commit a form of ‘ecological suicide’. Evaluation of a set of amphiphilic PK analogs with a diverse array of hydrophobic groups of the formula HR-Suc-FTPRLa led to the identification of analog T-63 (HR=Decyl) that increased the extent of diapause termination by a factor of 70% when applied topically to newly emerged pupae. Another biostablePK analog PK-Oic-1 featured anti-feedant and aphicidal properties that matched the potency of some commercial aphicides. Native PK showed no significant activity. The aphicidal effects were blocked by a new PEGylated PK antagonist analog PK-dF-PEG4, suggesting that the activity is mediated by a PK/PBAN receptor and therefore indicative of a novel and selective mode-of-action. Using a novel transPro mimetic motif (dihydroimidazole; ‘Jones’) developed in previous BARD-sponsored work, the first antagonist for the diapause hormone (DH), DH-Jo, was developed and shown to block over 50% of H. zea pupal diapause termination activity of native DH. This novel antagonist development strategy may be applicable to other invertebrate and vertebrate hormones that feature a transPro in the active core. The research identifies a critical component of the antagonist biophore for this PK/PBAN receptor subtype, i.e. a trans-oriented Pro. Additional work led to the molecular cloning and functional characterization of the DH receptor from H. zea, allowing for the discovery of three other DH antagonist analogs: Drosophila ETH, a β-AA analog, and a dF analog. The receptor experiments identified an agonist (DH-2Abf-dA) with a maximal response greater than native DH. ‘Deconvolution’ of a rationally-designed nonpeptide heterocyclic combinatorial library with a cyclic bis-guanidino (BG) scaffold led to discovery of several members that elicited activity in a pupariation acceleration assay, and one that also showed activity in an H. zea diapause termination assay, eliciting a maximal response of 90%. Molecular cloning and functional characterization of a CAP2b antidiuretic receptor from the kissing bug (R. prolixus) as well as the first CAP2b and PK receptors from a tick was also achieved. Notably, the PK/PBAN-like receptor from the cattle fever tick is unique among known PK/PBAN and CAP2b receptors in that it can interact with both ligand types, providing further evidence for an evolutionary relationship between these two NP families. In the course of the granting period we also managed to clone the PK/PBAN-R of H. peltigera, to express it and the S. littoralis-R Sf-9 cells and to evaluate their interaction with a variety of PK/PBAN ligands. In addition, three functional microplate assays in a HTS format have been developed: a cell-membrane competitive ligand binding assay; a Ca flux assay and a whole cell cAMP ELISA. The Ca flux assay has been used for receptor characterization due to its extremely high sensitivity. Computer homology studies were carried out to predict both receptor’s SAR and based on this analysis 8 mutants have been generated. The bioavailability of small linear antagonistic peptides has been evaluated and was found to be highly effective as sex pheromone biosynthesis inhibitors. The activity of 11 new amphiphilic analogs has also been evaluated. Unfortunately, due to a problem with the Heliothis moth colony we were unable to select those with pheromonotropic antagonistic activity and further check their bioavailability. Six peptides exhibited some melanotropic antagonistic activity but due to the low inhibitory effect the peptides were not further tested for bioavailability in S. littoralis larvae. Despite the fact that no new antagonistic peptides were discovered in the course of this granting period the results contribute to a better understanding of the interaction of the PK/PBAN family of Nps with their receptors, provided several HT assays for screening of libraries of various origin for presence of PK/PBAN-Ragonists and antagonists and provided important practical information for the further design of new, peptide-based insecticide prototypes aimed at the disruption of key neuroendocrine physiological functions in pest insects.

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