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Journal articles on the topic 'T-cell receptor'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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

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2

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

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6

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 expre

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7

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.

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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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10

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 rec

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11

Sommermeyer, Daniel, Julia Neudorfer, Monika Weinhold, et al. "Designer T cells by T cell receptor replacement." European Journal of Immunology 36, no. 11 (2006): 3052–59. http://dx.doi.org/10.1002/eji.200636539.

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12

Meeks, Christian Matthew, and Christopher G. Horton. "Modulation of CD4+ T cell polarization using non-canonical co-receptors." Journal of Immunology 198, no. 1_Supplement (2017): 150.15. http://dx.doi.org/10.4049/jimmunol.198.supp.150.15.

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Abstract CD4+ T helper cells are a diverse group of cells promoting target cell death and production of antibodies. These cells acquire one of several fates following signals through the T cell receptor, co-receptors, and cytokines. The cytokine requirements inducing the polarization of T cell fate has been heavily evaluated and reasonably well defined. However, the influence provided by co-receptors has not been completely elucidated. Traditionally, in vitro T cell polarization assays utilize CD28 stimulation as the primary co-receptor signal required for differentiation. Others have observed

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13

Simon, Bianca, Dennis C. Harrer, Beatrice Schuler-Thurner, Gerold Schuler, and Ugur Uslu. "Arming T Cells with a gp100-Specific TCR and a CSPG4-Specific CAR Using Combined DNA- and RNA-Based Receptor Transfer." Cancers 11, no. 5 (2019): 696. http://dx.doi.org/10.3390/cancers11050696.

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Tumor cells can develop immune escape mechanisms to bypass T cell recognition, e.g., antigen loss or downregulation of the antigen presenting machinery, which represents a major challenge in adoptive T cell therapy. To counteract these mechanisms, we transferred not only one, but two receptors into the same T cell to generate T cells expressing two additional receptors (TETARs). We generated these TETARs by lentiviral transduction of a gp100-specific T cell receptor (TCR) and subsequent electroporation of mRNA encoding a second-generation CSPG4-specific chimeric antigen receptor (CAR). Followi

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14

Barber, Amorette. "103 Inclusion of a Dap10 costimulatory domain enhances anti-tumor efficacy of chimeric PD1-expressing T cells in multiple types of solid tumors." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A114. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0103.

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BackgroundAdoptive transfer of T cells is a promising anti-tumor therapy for many cancers. To enhance tumor recognition by T cells, chimeric antigen receptors (CAR) consisting of signaling domains fused to receptors that recognize tumor antigens can be expressed in T cells. One receptor that is a prospective target for a new chimeric antigen receptor is PD1 because the ligands for the PD1 receptor are expressed on many cancer types. Therefore, we developed a murine chimeric PD1 receptor (chPD1) consisting of the PD1 receptor extracellular domain and the activation domain of CD3 zeta. In additi

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Robson MacDonald, H., Rosemary K. Lees, and Werner Held. "Developmentally Regulated Extinction of Ly-49 Receptor Expression Permits Maturation and Selection of NK1.1+ T Cells." Journal of Experimental Medicine 187, no. 12 (1998): 2109–14. http://dx.doi.org/10.1084/jem.187.12.2109.

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Clonally distributed inhibitory receptors negatively regulate natural killer (NK) cell function via specific interactions with allelic forms of major histocompatibility complex (MHC) class I molecules. In the mouse, the Ly-49 family of inhibitory receptors is found not only on NK cells but also on a minor (NK1.1+) T cell subset. Using Ly-49 transgenic mice, we show here that the development of NK1.1+ T cells, in contrast to NK or conventional T cells, is impaired when their Ly-49 receptors engage self-MHC class I molecules. Impaired NK1.1+ T cell development in transgenic mice is associated wi

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Mekala, Divya J., and Terrence L. Geiger. "Immunotherapy of autoimmune encephalomyelitis with redirected CD4+CD25+ T lymphocytes." Blood 105, no. 5 (2005): 2090–92. http://dx.doi.org/10.1182/blood-2004-09-3579.

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AbstractWe developed an approach that increases CD4+CD25+ regulatory T-cell potency by antigen-specifically redirecting them against pathologic T lymphocytes. The regulatory cells are transgenically modified with chimeric receptors that link antigen–major histocompatibility complex (MHC) extracellular and transmembrane domains with the cytoplasmic signaling tail of T-cell receptor ζ (TCR-ζ). The receptors' antigen-MHC recognizes the TCR of cognate T lymphocytes. Receptor engagement stimulates the receptor-modified T cell (RMTC) through the linked ζ chain. CD4+CD25+ RMTCs expressing a myelin ba

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17

Zhu, Yuwen, Alessandro Paniccia, Alexander C. Schulick, et al. "Identification of CD112R as a novel checkpoint for human T cells." Journal of Experimental Medicine 213, no. 2 (2016): 167–76. http://dx.doi.org/10.1084/jem.20150785.

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T cell immunoglobulin and ITIM domain (TIGIT) and CD226 emerge as a novel T cell cosignaling pathway in which CD226 and TIGIT serve as costimulatory and coinhibitory receptors, respectively, for the ligands CD155 and CD112. In this study, we describe CD112R, a member of poliovirus receptor–like proteins, as a new coinhibitory receptor for human T cells. CD112R is preferentially expressed on T cells and inhibits T cell receptor–mediated signals. We further identify that CD112, widely expressed on antigen-presenting cells and tumor cells, is the ligand for CD112R with high affinity. CD112R compe

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18

Guilbault, Benoit, and Robert J. Kay. "RasGRP1 Sensitizes an Immature B Cell Line to Antigen Receptor-induced Apoptosis." Journal of Biological Chemistry 279, no. 19 (2004): 19523–30. http://dx.doi.org/10.1074/jbc.m314273200.

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RasGRP1 is a guanine nucleotide exchange factor that activates Ras GTPases and is activated downstream of antigen receptors on both T and B lymphocytes. Ras-GRP1 provides signals to immature T cells that confer survival and proliferation, but RasGRP1 also promotes T cell receptor-mediated deletion of mature T cells. We used the WEHI-231 cell line as an experimental system to determine whether RasGRP1 can serve as a quantitative modifier of B cell receptor-induced deletion of immature B cells. A 2-fold elevation in RasGRP1 expression markedly increased apoptosis of WEHI-231 cells following B ce

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19

Joyce, David E., Yan Chen, Rochelle A. Erger, Gary A. Koretzky, and Steven R. Lentz. "Functional Interactions Between the Thrombin Receptor and the T-Cell Antigen Receptor in Human T-Cell Lines." Blood 90, no. 5 (1997): 1893–901. http://dx.doi.org/10.1182/blood.v90.5.1893.

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Abstract The proteolytically activated thrombin receptor (TR) is expressed by T lymphocytes, which suggests that thrombin may modulate T-cell activation at sites of hemostatic stress. We examined the relationship between TR function and T-cell activation in the Jurkat human T-cell line and in T-cell lines with defined defects in T-cell antigen receptor (TCR) function. Stimulation with thrombin or the synthetic TR peptide SFLLRN produced intracellular Ca2+ transients in Jurkat cells. As the concentration of TR agonist was increased, peak Ca2+ mobilization increased, but influx of extracellular

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20

Huang, Jun. "Lattice light-sheet microscopy Multi-Dimensional Analyses (LaMDA) of T-cell receptor dynamics predict T-cell signaling states." Journal of Immunology 204, no. 1_Supplement (2020): 80.10. http://dx.doi.org/10.4049/jimmunol.204.supp.80.10.

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Abstract Cell surface receptors dynamically change in response to cell signaling, but a direct linkage between receptor dynamics and cell state has not been established. Here we report the development of lattice light-sheet microscopy multi-dimensional analyses (LaMDA), a pipeline that combines high spatiotemporal-resolution four-dimensional lattice light-sheet microscopy, machine learning, and diffusion maps to analyze T-cell receptor (TCR) dynamics and predict T-cell signaling states without the need for complex biochemical measurements. LaMDA images thousands of TCR microclusters on the sur

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21

Zhang, Peng-Fei, Chuang Wang, Le Zhang, and Qiu Li. "Reversing chemokine/chemokine receptor mismatch to enhance the antitumor efficacy of CAR-T cells." Immunotherapy 14, no. 6 (2022): 459–73. http://dx.doi.org/10.2217/imt-2021-0228.

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Currently, the antitumor efficacy of chimeric antigen receptor T cells in solid tumors is modest. Both chemokines and their receptors play a key role in the proliferation of cancer cells, tumor angiogenesis, organ-selective metastasis and migration of immune cells to solid tumors. Unfortunately, frequent chemokine/chemokine receptor ‘mismatch’ between effector cells and the tumor microenvironment results in inefficient T-cell infiltration and antitumor efficacy. Thus, reversing the ‘mismatch’ of chemokines and chemokine receptors appears to be a promising method for promoting T-cell infiltrati

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22

Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "CAR T Cells: Precision Cancer Immunotherapy." Indonesian Biomedical Journal 10, no. 3 (2018): 203–16. http://dx.doi.org/10.18585/inabj.v10i3.635.

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BACKGROUND: Current cancer drugs and treatments are aiming at eradicating tumor cells, but often are more toxic then effective, killing also the normal cells and not selectively the tumor cells. There is good personalized cancer therapy that involves administration to the cancer-bearing host of immune cells with direct anticancer activity, which called adoptive cell therapy (ACT). A review of the unique biology of T cell therapy and of recent clinical experience compels a reassessment of target antigens that traditionally have been viewed from the perspective of weaker immunotherapeutic modali

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23

Lin, Joseph, and Arthur Weiss. "T cell receptor signalling." Journal of Cell Science 114, no. 2 (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 (2021): 71.4–72. http://dx.doi.org/10.1126/science.373.6550.71-d.

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25

Marrack, P., and J. Kappler. "The T cell receptor." Science 238, no. 4830 (1987): 1073–79. http://dx.doi.org/10.1126/science.3317824.

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26

McGargill, Maureen A., and Kristin A. Hogquist. "T cell receptor editing." Immunology Letters 75, no. 1 (2000): 27–31. http://dx.doi.org/10.1016/s0165-2478(00)00282-0.

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27

Mak, T. W. "T cell antigen receptor." Leukemia Research 10, no. 1 (1986): 84. http://dx.doi.org/10.1016/0145-2126(86)90120-7.

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Potter, C. "The T-Cell Receptor." Journal of Clinical Pathology 42, no. 3 (1989): 334. http://dx.doi.org/10.1136/jcp.42.3.334-a.

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HAUSER, STEPHEN L. "T-Cell Receptor Genes." Annals of the New York Academy of Sciences 756, no. 1 T-Cell Recept (1995): 233–40. http://dx.doi.org/10.1111/j.1749-6632.1995.tb44521.x.

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30

Lieberman, Judy, and David H. Raulet. "T cell gamma receptor." Immunologic Research 6, no. 4 (1987): 288–93. http://dx.doi.org/10.1007/bf02935523.

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31

Tual, Margaux, Angélique Bellemare-Pelletier, Susan Moore, et al. "MARC, a novel modular chimeric antigen receptor, improves T cell-based cancer immunotherapies by preventing early T cell exhaustion and enhancing persistence." Journal for ImmunoTherapy of Cancer 13, no. 4 (2025): e011829. https://doi.org/10.1136/jitc-2025-011829.

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BackgroundChimeric antigen receptor T cell (CAR-T)-based immunotherapies have reshaped the therapeutic landscape of cancer treatment, in particular for patients afflicted with leukemia. However, defects in CAR behaviors and clinical complications have hindered their widespread application across diverse cancer types. Chief among these defects is high tonic signaling, absent in native activating immune receptors, which accelerates T cell exhaustion and undermines treatment efficacy. We hypothesized that these limitations arise because current CAR architectures fail to replicate the modular desi

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Padovan, E., G. Casorati, P. Dellabona, S. Meyer, M. Brockhaus, and A. Lanzavecchia. "Expression of two T cell receptor alpha chains: dual receptor T cells." Science 262, no. 5132 (1993): 422–24. http://dx.doi.org/10.1126/science.8211163.

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MELMS, A., J. R. OKSENBERG, G. MALCHEREK, et al. "T-Cell Receptor Gene Usage of Acetylcholine Receptor-specific T-Helper Cells." Annals of the New York Academy of Sciences 681, no. 1 Myasthenia Gr (1993): 313–14. http://dx.doi.org/10.1111/j.1749-6632.1993.tb22904.x.

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Alcázar, Isabela, Miriam Marqués, Amit Kumar та ін. "Phosphoinositide 3–kinase γ participates in T cell receptor–induced T cell activation". Journal of Experimental Medicine 204, № 12 (2007): 2977–87. http://dx.doi.org/10.1084/jem.20070366.

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Class I phosphoinositide 3–kinases (PI3Ks) constitute a family of enzymes that generates 3-phosphorylated polyphosphoinositides at the cell membrane after stimulation of protein tyrosine (Tyr) kinase–associated receptors or G protein–coupled receptors (GPCRs). The class I PI3Ks are divided into two types: class IA p85/p110 heterodimers, which are activated by Tyr kinases, and the class IB p110γ isoform, which is activated by GPCR. Although the T cell receptor (TCR) is a protein Tyr kinase–associated receptor, p110γ deletion affects TCR-induced T cell stimulation. We examined whether the TCR ac

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Steverding, Dietmar. "Cycle Numbers of Cell Surface Recycling Receptors." Receptors 2, no. 2 (2023): 160–65. http://dx.doi.org/10.3390/receptors2020010.

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The cycle number (nc) of a recycling receptor is defined as the average number of round trips (cell surface–endosome–cell surface) the receptor can make before it is degraded. This characteristic parameter of recycling receptors can be easily determined from the receptor’s half-life (t½, the time in which 50% of the receptor is degraded) and cycling time (Tc, the time a receptor needs to complete a round trip). Relationship analyses revealed that nc increases linearly with increasing t½ and decreases exponentially with increasing Tc. For commonly observed t½ and Tc values, it was calculated th

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Hansenne, I., G. Rasier, Ch Charlet-renard, et al. "Neurohypophysial Receptor Gene Expression by Thymic T Cell Subsets and Thymic T Cell Lymphoma Cell Lines." Clinical and Developmental Immunology 11, no. 1 (2004): 45–51. http://dx.doi.org/10.1080/10446670410001670481.

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Abstract Neurohypophysial oxytocin (OT) and vasopressin (VP) genes are transcribed in thymic epithelium, while immature T lymphocytes express functional neurohypophysial receptors. Neurohypophysial receptors belong to the G protein-linked seven-transmembrane receptor superfamily and are encoded by four distinct genes,OTR,V1R,V2RandV3R. The objective of this study was to identify the nature of neurohypophysial receptor in thymic T cell subsets purified by immunomagnetic selection, as well as in murine thymic lymphoma cell lines RL12-NP and BW5147.OTRis transcribed in all thymic T cell subsets a

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Kempkes, B., E. Palmer, S. Martin, et al. "Predominant T cell receptor gene elements in TNP-specific cytotoxic T cells." Journal of Immunology 147, no. 8 (1991): 2467–73. http://dx.doi.org/10.4049/jimmunol.147.8.2467.

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Abstract H-2b class I-restricted, TNP-specific CTL clones were obtained by limiting dilution cloning of either short term polyclonal CTL lines or spleen cells of TNP-immunized mice directly ex vivo. Sequence analyses of mRNA coding for TCR alpha- and beta-chains of 11 clones derived from CTL lines from individual C57BL/6 mice revealed that all of them expressed unique but clearly nonrandom receptor structures. Five alpha-chains (45%) employed V alpha 10 gene elements, and four of those (36%) were associated with J beta 2.6-expressing beta-chains. The alpha-chains from these four TCR, moreover,

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Greenbaum, Uri, Ecaterina I. Dumbrava, Amadeo B. Biter, Cara L. Haymaker, and David S. Hong. "Engineered T-cell Receptor T Cells for Cancer Immunotherapy." Cancer Immunology Research 9, no. 11 (2021): 1252–61. http://dx.doi.org/10.1158/2326-6066.cir-21-0269.

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Abstract Engineering immune cells to target cancer is a rapidly advancing technology. The first commercial products, chimeric-antigen receptor (CAR) T cells, are now approved for hematologic malignancies. However, solid tumors pose a greater challenge for cellular therapy, in part because suitable cancer-specific antigens are more difficult to identify and surrounding healthy tissues are harder to avoid. In addition, impaired trafficking of immune cells to solid tumors, the harsh immune-inhibitory microenvironment, and variable antigen density and presentation help tumors evade immune cells ta

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Radtanakatikanon, Araya, Peter F. Moore, Stefan M. Keller, and William Vernau. "Novel clonality assays for T cell lymphoma in cats targeting the T cell receptor beta, T cell receptor delta, and T cell receptor gamma loci." Journal of Veterinary Internal Medicine 35, no. 6 (2021): 2865–75. http://dx.doi.org/10.1111/jvim.16288.

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Li, Zhuqing, Maria J. Calzada, John M. Sipes та ін. "Interactions of thrombospondins with α4β1 integrin and CD47 differentially modulate T cell behavior". Journal of Cell Biology 157, № 3 (2002): 509–19. http://dx.doi.org/10.1083/jcb.200109098.

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Thrombospondin (TSP)-1 has been reported to modulate T cell behavior both positively and negatively. We found that these opposing responses arise from interactions of TSP1 with two different T cell receptors. The integrin α4β1 recognizes an LDVP sequence in the NH2-terminal domain of TSP1 and was required for stimulation of T cell adhesion, chemotaxis, and matrix metalloproteinase gene expression by TSP1. Recognition of TSP1 by T cells depended on the activation state of α4β1 integrin, and TSP1 inhibited interaction of activated α4β1 integrin on T cells with its counter receptor vascular cell

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Chen, Yuehong, Jianhong Sun, Huan Liu, Geng Yin, and Qibing Xie. "Immunotherapy Deriving from CAR-T Cell Treatment in Autoimmune Diseases." Journal of Immunology Research 2019 (December 31, 2019): 1–9. http://dx.doi.org/10.1155/2019/5727516.

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Chimeric antigen receptor T (CAR-T) cells are T cells engineered to express specific synthetic antigen receptors that can recognize antigens expressed by tumor cells, which after the binding of these antigens to the receptors are eliminated, and have been adopted to treat several kinds of malignancies. Autoimmune diseases (AIDs), a class of chronic disease conditions, can be broadly separated into autoantibody-mediated and T cell-mediated diseases. Treatments for AIDs are focused on restoring immune tolerance. However, current treatments have little effect on immune tolerance inverse; even the

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Lefrançois, Leo, Terrence A. Barrett, Wendy L. Havran та Lynn Puddington. "Developmental expression of the αIELβ7 integrin on T cell receptor γδ and T cell receptor αβ T cells". European Journal of Immunology 24, № 3 (1994): 635–40. http://dx.doi.org/10.1002/eji.1830240322.

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Janssen, O., S. Wesselborg, B. Heckl-Ostreicher, et al. "T cell receptor/CD3-signaling induces death by apoptosis in human T cell receptor gamma delta + T cells." Journal of Immunology 146, no. 1 (1991): 35–39. http://dx.doi.org/10.4049/jimmunol.146.1.35.

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Abstract mAb directed against the TCR/CD3 complex activate resting T cells. However, TCR/CD3 signaling induces death by apoptosis in immature (CD4+CD8+) murine thymocytes and certain transformed leukemic T cell lines. Here we show that anti-TCR and anti-CD3 mAb induce growth arrest of cloned TCR-gamma delta + T cells in the presence of IL-2. In the absence of exogenous IL-2, however, the very same anti-TCR/CD3 mAb stimulated gamma delta (+)-clones to proliferation and IL-2 production. In the presence of exogenous IL-2, anti-TCR/CD3 mAb induced the degradation of DNA into oligosomal bands of ap

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Biffen, M., and D. R. Alexander. "Mobilization of intracellular Ca2+ by adenine nucleotides in human T-leukaemia cells: evidence for ADP-specific and P2y-purinergic receptors." Biochemical Journal 304, no. 3 (1994): 769–74. http://dx.doi.org/10.1042/bj3040769.

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The expression of purinergic receptors on human T-cells was investigated and the receptors were shown to be functionally coupled to intracellular signals in two out of eight T-leukaemia cell-lines. Addition of adenine nucleotides resulted in mobilization of intracellular Ca2+ in HPB-ALL cells and a cell line (CB1) recently isolated from a patient with T-acute lymphoblastic leukaemia. Of a range of nucleotides tested only ADP and ATP elevated intracellular levels of Ca2+, with ADP being the more potent agonist. Ca2+ mobilization by ATP was accompanied by increased inositol phosphate production

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Hashimoto, Y., K. Yui, D. Littman, and M. I. Greene. "T-cell receptor genes in autoimmune mice: T-cell subsets have unexpected T-cell receptor gene programs." Proceedings of the National Academy of Sciences 84, no. 16 (1987): 5883–87. http://dx.doi.org/10.1073/pnas.84.16.5883.

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Scheurich, P., B. Thoma, U. Ucer, and K. Pfizenmaier. "Immunoregulatory activity of recombinant human tumor necrosis factor (TNF)-alpha: induction of TNF receptors on human T cells and TNF-alpha-mediated enhancement of T cell responses." Journal of Immunology 138, no. 6 (1987): 1786–90. http://dx.doi.org/10.4049/jimmunol.138.6.1786.

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Abstract The expression of specific tumor necrosis factor (TNF) membrane receptors and biological effects of recombinant TNF (rTNF)-alpha on normal human T lymphocytes were studied. Although resting T cells lacked specific binding capacity for rTNF-alpha, high affinity (Kd 70 pM) TNF receptors were de novo induced upon primary activation of T cells. Comparison of TNF receptor expression with that of high affinity interleukin 2 (IL-2) and interferon-gamma (IFN-gamma) receptors, respectively, revealed similarities to IL 2-receptor expression with respect to kinetics of induction. However, maximu

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Li, Hao-Kang, Tai-Sheng Wu, Yi-Chiu Kuo, et al. "A Novel Allogeneic Rituximab-Conjugated Gamma Delta T Cell Therapy for the Treatment of Relapsed/Refractory B-Cell Lymphoma." Cancers 15, no. 19 (2023): 4844. http://dx.doi.org/10.3390/cancers15194844.

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Chimeric antigen receptor T cell (CAR-T) therapy has been applied in the treatment of B-cell lymphoma; however, CAR-T manufacturing requires virus- or non-virus-based genetic modification, which causes high manufacturing costs and potential safety concerns. Antibody–cell conjugation (ACC) technology, which originated from bio-orthogonal click chemistry, provides an efficient approach for arming immune cells with cancer-targeting antibodies without genetic modification. Here, we applied ACC technology in Vγ9Vδ2 T (γδ2 T) cells to generate a novel off-the-shelf CD20-targeting cell therapy ACE183

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Young, Mary H., Garnet Navarro, Peter Askovich, and Alan Aderem. "T cell receptor signaling and Toll-like receptor signaling converge to amplify T cell responses." Journal of Immunology 196, no. 1_Supplement (2016): 128.5. http://dx.doi.org/10.4049/jimmunol.196.supp.128.5.

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Abstract Toll-like receptors (TLRs) are an essential part of the innate immune system. Their function on antigen presenting cells helps drive efficient T cell responses to pathogens. However, T cells also express several TLRs. Additionally, many of the downstream signaling components of TLRs are shared with those of the T cell receptor. Our hypothesis is that these two pathways work in concert to exert unique and potent T cell responses. We have found that several TLRs are able to enhance T cell responses, including TLR3, TLR4, TLR7, and TLR9. We have found that TLR7 signaling, in particular,

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Kees, UR. "Phorbol ester induces expression and function of interleukin-2 receptors on a human leukemic cell line with a T-cell precursor phenotype." Blood 72, no. 5 (1988): 1524–29. http://dx.doi.org/10.1182/blood.v72.5.1524.1524.

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Abstract We show here that a human leukemic cell line, PER-117, bearing the markers of a T-cell precursor phenotype, can be induced to express receptors for interleukin-2 (IL-2). These IL-2 receptors could be demonstrated to mediate a physiologic response to the lymphokine for which the high-affinity form of the IL-2 receptor appears to be essential. The phenotype of PER-117 cells corresponds to the earliest identifiable stage of T-cell differentiation, which is defined by the lack of the T3-T-cell receptor complex and the presence of the 40 Kd protein recognized by monoclonal antibodies of th

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Kees, UR. "Phorbol ester induces expression and function of interleukin-2 receptors on a human leukemic cell line with a T-cell precursor phenotype." Blood 72, no. 5 (1988): 1524–29. http://dx.doi.org/10.1182/blood.v72.5.1524.bloodjournal7251524.

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Abstract:

We show here that a human leukemic cell line, PER-117, bearing the markers of a T-cell precursor phenotype, can be induced to express receptors for interleukin-2 (IL-2). These IL-2 receptors could be demonstrated to mediate a physiologic response to the lymphokine for which the high-affinity form of the IL-2 receptor appears to be essential. The phenotype of PER-117 cells corresponds to the earliest identifiable stage of T-cell differentiation, which is defined by the lack of the T3-T-cell receptor complex and the presence of the 40 Kd protein recognized by monoclonal antibodies of the CD7 gro

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