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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: 15 June 2025

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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 (2019): 1384–90. http://dx.doi.org/10.2169/naika.108.1384.

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Moskalev, Alexander V., Boris Yu Gumilevskiy, Vasiliy Ya Apchel, and Vasiliy N. Cygan. "T-cell receptor family, signal transduction, and transcription factors in T-cell immune response." Bulletin of the Russian Military Medical Academy 27, no. 1 (2025): 135–46. https://doi.org/10.17816/brmma636850.

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This study investigated signal transduction in T-lymphocytes, whose cell receptors are categorized into several groups based on their signaling mechanisms and the intracellular biochemical pathways they activate, including modular signaling proteins and adapter molecules that perform scaffolding or catalytic functions. Adapter proteins facilitate signaling complexes by linking various enzymes. Immune receptors, which are composed of integral membrane proteins from the immunoglobulin superfamily, interact with specific tyrosine-containing motifs within transmembrane signaling proteins in their cytoplasmic domains. The intensity of T-cell receptor signaling influences the development and activation of T-lymphocytes. Signal transduction is regulated by coreceptor activation and suppressed by inhibitory receptors. The interaction between T-cell receptors and major histocompatibility complex molecules induces coreceptor clustering and tyrosine phosphorylation of immunoreceptor tyrosine-based activation motifs within the cluster of differentiation 3 complex. Protein and lipid phosphorylation is a key regulatory mechanism in T-cell receptor and coreceptor signaling. Activated zeta-chain-associated protein kinase 70 phosphorylates adapter proteins, promoting interactions with downstream signaling molecules. G-proteins stimulate mitogen-activated protein kinases, which activate transcription factors. Phospholipase C activates T-cell transcription factors, resulting in enhanced gene transcription. T-cell receptor signal modulation is mediated by protein tyrosine phosphatases, which dephosphorylate tyrosine residues on signaling proteins, inhibiting T-cell receptor-mediated signal transduction.

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Rabin, Ronald L., Matthew K. Park, Fang Liao, Ruth Swofford, David Stephany, and Joshua M. Farber. "Chemokine Receptor Responses on T Cells Are Achieved Through Regulation of Both Receptor Expression and Signaling." Journal of Immunology 162, no. 7 (1999): 3840–50. http://dx.doi.org/10.4049/jimmunol.162.7.3840.

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Abstract To address the issues of redundancy and specificity of chemokines and their receptors in lymphocyte biology, we investigated the expression of CC chemokine receptors CCR1, CCR2, CCR3, CCR5, CXCR3, and CXCR4 and responses to their ligands on memory and naive, CD4 and CD8 human T cells, both freshly isolated and after short term activation in vitro. Activation through CD3 for 3 days had the most dramatic effects on the expression of CXCR3, which was up-regulated and functional on all T cell populations including naive CD4 cells. In contrast, the effects of short term activation on expression of other chemokine receptors was modest, and expression of CCR2, CCR3, and CCR5 on CD4 cells was restricted to memory subsets. In general, patterns of chemotaxis in the resting cells and calcium responses in the activated cells corresponded to the patterns of receptor expression among T cell subsets. In contrast, the pattern of calcium signaling among subsets of freshly isolated cells did not show a simple correlation with receptor expression, so the propensity to produce a global rise in the intracellular calcium concentration differed among the various receptors within a given T cell subset and for an individual receptor depending on the cell where it was expressed. Our data suggest that individual chemokine receptors and their ligands function on T cells at different stages of T cell activation/differentiation, with CXCR3 of particular importance on newly activated cells, and demonstrate T cell subset-specific and activation state-specific responses to chemokines that are achieved by regulating receptor signaling as well as receptor expression.

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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 (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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Rosenberg, Kenneth M., and Nevil J. Singh. "Subset-specific neurotransmitter receptor expression tunes T cell activation." Journal of Immunology 200, no. 1_Supplement (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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OMOTO, K., Y. Y. KONG, K. NOMOTO та ін. "Sensitization of T-cell receptor-αβ+ T cells recovered from long-term T-cell receptor downmodulation". Immunology 88, № 2 (1996): 230–37. http://dx.doi.org/10.1111/j.1365-2567.1996.tb00009.x.

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Grunewald, Johan, Ylva Kaiser, Mahyar Ostadkarampour, et al. "T-cell receptor–HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis." European Respiratory Journal 47, no. 3 (2015): 898–909. http://dx.doi.org/10.1183/13993003.01209-2015.

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In pulmonary sarcoidosis, CD4+ T-cells expressing T-cell receptor Vα2.3 accumulate in the lungs of HLA-DRB1*03+ patients. To investigate T-cell receptor-HLA-DRB1*03 interactions underlying recognition of hitherto unknown antigens, we performed detailed analyses of T-cell receptor expression on bronchoalveolar lavage fluid CD4+ T-cells from sarcoidosis patients.Pulmonary sarcoidosis patients (n=43) underwent bronchoscopy with bronchoalveolar lavage. T-cell receptor α and β chains of CD4+ T-cells were analysed by flow cytometry, DNA-sequenced, and three-dimensional molecular models of T-cell receptor-HLA-DRB1*03 complexes generated.Simultaneous expression of Vα2.3 with the Vβ22 chain was identified in the lungs of all HLA-DRB1*03+ patients. Accumulated Vα2.3/Vβ22-expressing T-cells were highly clonal, with identical or near-identical Vα2.3 chain sequences and inter-patient similarities in Vβ22 chain amino acid distribution. Molecular modelling revealed specific T-cell receptor-HLA-DRB1*03-peptide interactions, with a previously identified, sarcoidosis-associated vimentin peptide, (Vim)429–443 DSLPLVDTHSKRTLL, matching both the HLA peptide-binding cleft and distinct T-cell receptor features perfectly.We demonstrate, for the first time, the accumulation of large clonal populations of specific Vα2.3/Vβ22 T-cell receptor-expressing CD4+ T-cells in the lungs of HLA-DRB1*03+ sarcoidosis patients. Several distinct contact points between Vα2.3/Vβ22 receptors and HLA-DRB1*03 molecules suggest presentation of prototypic vimentin-derived peptides.

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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.<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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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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Gérard, Lefranc, ed. The T cell receptor factsbook. Academic Press, 2001.

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Liu, Chaohong, ed. T-Cell Receptor Signaling. 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. University of Birmingham, 1993.

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

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

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

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van den Elsen, Peter J. The Human T-Cell Receptor Repertoire and Transplantation. 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. 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. 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. University of Manchester, 1996.

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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. 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. 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, et al. "The T-Cell Receptor." In Investigation and Exploitation of Antibody Combining Sites. 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. ASM Press, 2015. http://dx.doi.org/10.1128/9781555816148.ch13.

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Haskins, Kathryn, Neal Roehm, Charles Hannum, et al. "The Murine T Cell Receptor." In Human T Cell Clones. 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. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64686-8_13.

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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. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5406-2_5.

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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. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_7.

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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. 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. 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"

1

Fang, Xing, Chenpeng Yu, Shiye Tian, and Hui Liu. "A large language model for predicting T cell receptor-antigen binding specificity." In 2024 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2024. https://doi.org/10.1109/bibm62325.2024.10822735.

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Wang, Haoyan, Yifei Huang, and Tianyi Zang. "MFTEP: A Multimodal Fusion Deep Learning Framework for T Cell Receptor-epitope Interaction Prediction." In 2024 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2024. https://doi.org/10.1109/bibm62325.2024.10821958.

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de Rooij, MAJ, DM Steen, D. Remst, et al. "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. ACM, 2020. http://dx.doi.org/10.1145/3397391.3397451.

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Sherwood, Anna M., Harlan Robins, Jonathan R. Fromm, et al. "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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Davis, Nicholas S., Catherine Leites, Helicia Paz, et al. "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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Wu, Ling, Joanna Brzostek, Shvetha Sankaran, et al. "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, et al. "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. ACM, 2020. http://dx.doi.org/10.1145/3403782.3403802.

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Donaghey, Julie, Philippe Kieffer-Kwon, Troy Patterson, et al. "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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Reports on the topic "T-cell receptor"

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Knouse, Michael. Chimeric Antigen Receptor T Cell Therapy: A Review. Iowa State University, 2018. http://dx.doi.org/10.31274/cc-20240624-355.

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Iqbal, Fatiha. Chimeric Antigen Receptor (CAR) T Cell Immunotherapies for Leukemias and Lymphomas. Iowa State University, 2019. http://dx.doi.org/10.31274/cc-20240624-354.

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Weinberg, Andrew D. Tumor Specific CD4+ T-Cell Costimulation Through a Novel Receptor/Ligand Interaction. Defense Technical Information Center, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada553485.

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Zhao, Kangjia, Jiwen Sun, Nanping Shen, et al. 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, 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. Defense Technical Information Center, 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. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada586024.

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