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Journal articles on the topic 'T-cell receptor'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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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 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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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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Marrack, P., and J. Kappler. "The T cell receptor." Science 238, no. 4830 (November 20, 1987): 1073–79. http://dx.doi.org/10.1126/science.3317824.

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12

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

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13

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

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14

Potter, C. "The T-Cell Receptor." Journal of Clinical Pathology 42, no. 3 (March 1, 1989): 334. http://dx.doi.org/10.1136/jcp.42.3.334-a.

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15

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

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16

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

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17

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 (April 1, 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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18

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 (October 15, 1993): 422–24. http://dx.doi.org/10.1126/science.8211163.

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19

MELMS, A., J. R. OKSENBERG, G. MALCHEREK, R. SCHOEPFER, C. A. MÜLLER, J. LINDSTROM, and L. STEINMAN. "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 (June 1993): 313–14. http://dx.doi.org/10.1111/j.1749-6632.1993.tb22904.x.

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20

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 (November 2021): 2865–75. http://dx.doi.org/10.1111/jvim.16288.

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21

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 (November 1, 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 targeting cancer-specific antigens. To overcome these obstacles, T cells are being engineered to express defined T-cell receptors (TCR). Given that TCRs target intracellular peptides expressed on tumor MHC molecules, this provides an expanded pool of potential targetable tumor-specific antigens relative to the cell-surface antigens that are targeted by CAR T cells. The affinity of TCR T cells can be tuned to allow for better tumor recognition, even with varying levels of antigen presentation on the tumor and surrounding healthy tissue. Further enhancements to TCR T cells include improved platforms that enable more robust cell expansion and persistence; coadministration of small molecules that enhance tumor recognition and immune activation; and coexpression of cytokine-producing moieties, activating coreceptors, or mediators that relieve checkpoint blockade. Early-phase clinical trials pose logistical challenges involving production, large-scale manufacturing, and more. The challenges and obstacles to successful TCR T-cell therapy, and ways to overcome these and improve anticancer activity and efficacy, are discussed herein.

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22

Lefrançois, Leo, Terrence A. Barrett, Wendy L. Havran, and 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, no. 3 (March 1994): 635–40. http://dx.doi.org/10.1002/eji.1830240322.

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23

Janssen, O., S. Wesselborg, B. Heckl-Ostreicher, K. Pechhold, A. Bender, S. Schondelmaier, G. Moldenhauer, and D. Kabelitz. "T cell receptor/CD3-signaling induces death by apoptosis in human T cell receptor gamma delta + T cells." Journal of Immunology 146, no. 1 (January 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 approximately 200 bp length in cloned gamma delta + T cells. This pattern of DNA fragmentation is characteristic for the programmed cell death termed apoptosis. These results demonstrate that TCR/CD3 signaling can induce cell death in cloned gamma delta + T cells. In addition, this report is the first to show that apoptosis triggered by TCR/CD3 signaling is not restricted to CD4+CD8+ immature thymocytes and transformed leukemic T cell lines but can be also observed with IL-2-dependent normal (i.e., TCR-gamma delta +) T cells.

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24

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 (August 1, 1987): 5883–87. http://dx.doi.org/10.1073/pnas.84.16.5883.

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25

Alcázar, Isabela, Miriam Marqués, Amit Kumar, Emilio Hirsch, Matthias Wymann, Ana C. Carrera, and Domingo F. Barber. "Phosphoinositide 3–kinase γ participates in T cell receptor–induced T cell activation." Journal of Experimental Medicine 204, no. 12 (November 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 activates p110γ, as well as the consequences of interfering with p110γ expression or function for T cell activation. We found that after TCR ligation, p110γ interacts with Gαq/11, lymphocyte-specific Tyr kinase, and ζ-associated protein. TCR stimulation activates p110γ, which affects 3-phosphorylated polyphosphoinositide levels at the immunological synapse. We show that TCR-stimulated p110γ controls RAS-related C3 botulinum substrate 1 activity, F-actin polarization, and the interaction between T cells and antigen-presenting cells, illustrating a crucial role for p110γ in TCR-induced T cell activation.

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26

Kempkes, B., E. Palmer, S. Martin, A. von Bonin, K. Eichmann, B. Ortmann, and H. U. Weltzien. "Predominant T cell receptor gene elements in TNP-specific cytotoxic T cells." Journal of Immunology 147, no. 8 (October 15, 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, contained an acidic amino acid in position 93 of their N or J region-determined sequences. Clones isolated directly from spleen cells carried these types of receptors at lower frequency, 27% V alpha 10 and 19% J beta 2.6, indicating that bulk in vitro cultivation on Ag leads to selection for these particular receptors. However, even in TNP-specific CTL cloned directly ex vivo, V alpha 10 usage was increased about fivefold over that in Ag-independently activated T cells in H-2b mice (4 to 5%). The selection for V alpha 10/J beta 2.6-expressing cells was obtained repeatedly in other TNP-specific CTL lines from C57BL/6 mice but not in FITC-specific CTL from the same strain or in TNP-specific CTL lines from B10.BR (H-2k) or B10.D2 (H-2d) mice. We conclude from this (a) that the selection for V alpha 10/J beta 2.6+ T cells is driven by the complementarity of these receptors to a combination of TNP and MHC epitopes and (b) that predominant receptor structures reflect the existence of a surprisingly limited number of "T cell-relevant" hapten determinants on the surface of covalently TNP-modified cells.

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27

Shimada, Shinji. "T Cell Receptor Expression by Dendritic Epidermal T Cells." Journal of Dermatology 21, no. 11 (November 1994): 829–32. http://dx.doi.org/10.1111/j.1346-8138.1994.tb03297.x.

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28

Pacholczyk, Rafal, and Joanna Kern. "The T-cell receptor repertoire of regulatory T cells." Immunology 125, no. 4 (December 2008): 450–58. http://dx.doi.org/10.1111/j.1365-2567.2008.02992.x.

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29

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 (September 1, 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 Ca2+ decreased. TR signaling was enhanced in a TCR-negative Jurkat line and in T-cell lines deficient in the tyrosine kinase lck or the tyrosine phosphatase CD45, both of which are essential for normal TCR function. TCR cross-linking with anti-CD3 IgM desensitized TR signaling in Jurkat cells, but not in CD45-deficient cells. A proteinase-activated receptor (PAR-2)–specific agonist peptide, SLIGKV, produced small Ca2+ transients in both MEG-01 human megakaryocytic cells and Jurkat cells, but was less potent than the TR-specific agonist TFRIFD in both cell types. Like TR signaling, PAR-2 signaling was enhanced in TCR-negative or lck-deficient Jurkat clones. These findings provide evidence for functional cross-talk between proteolytically activated receptors and the TCR.

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30

Hansenne, I., G. Rasier, Ch Charlet-renard, M. P. Defresne, R. Greimers, C. Breton, J. J. Legros, V. Geenen, and H. Martens. "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 and T cell lines, whileV3Rtranscription is restricted to CD4+CD8+and CD8+thymic cells. NeitherV1RnorV2Rtranscripts are detected in any kind of T cells. The OTR protein was identified by immunocytochemistry on thymocytes freshly isolated from C57BL/6 mice. In murine fetal thymic organ cultures, a specific OTR antagonist does not modify the percentage of T cell subsets, but increases late T cell apoptosis further evidencing the involvement of OT/OTR signaling in the control of T cell proliferation and survival. According to these data,OTRandV3Rare differentially expressed during T cell ontogeny. Moreover, the restriction ofOTRtranscription to T cell lines derived from thymic lymphomas may be important in the context of T cell leukemia pathogenesis and treatment.

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31

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 (May 1, 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, synergizes with TCR activation and improves T cell effector functions. Priming T cells with synthetic and natural TLR7 ligands before TCR ligation further boosts T cell responses. The combination of TLR7 and TCR stimulation in T cells enhances cytokine production and proliferation in T cells. We identified several overlapping components between TLR7 and TCR activation pathways by gene expression, which may provide combinatorial increases in T cell activation. In addition, we found increases in anti-viral response pathways that are atypical in T cells. This response was unique to the combination of TLR and TCR stimuli. Thus, we wanted to determine if TLR7 signaling in T cells is important during an acute infection. During influenza, T cell-specific loss of TLR7 alters infection dynamics in the T cell population, resulting in significant activation delays and abnormalities. These findings show that TLR7 is important in normal T cell responses to viral infections. Understanding the contribution of TLR signaling to T cell activation will be useful in guiding enhanced vaccine strategies.

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32

Liu, Qi, Wenxuan Cai, Wei Zhang, and Yi Li. "Cancer immunotherapy using T-cell receptor engineered T cell." Annals of Blood 5 (March 2020): 5. http://dx.doi.org/10.21037/aob.2020.02.02.

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33

Davis, Mark M., and Pamela J. Bjorkman. "T-cell antigen receptor genes and T-cell recognition." Nature 334, no. 6181 (August 1, 1988): 395–402. http://dx.doi.org/10.1038/334395a0.

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Davis, Mark M., and Pamela J. Bjorkman. "T-cell antigen receptor genes and T-cell recognition." Nature 335, no. 6192 (October 1988): 744. http://dx.doi.org/10.1038/335744b0.

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35

Mori, Naoyoshi, Kuniyuki Oka, Yasuhiro Yoda, Tsukasa Abe, and Mizu Kojima. "T-Cell Receptor Expression in the T-Cell Malignancies." American Journal of Clinical Pathology 93, no. 4 (April 1, 1990): 495–501. http://dx.doi.org/10.1093/ajcp/93.4.495.

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36

Marelli-Berg, F. M., M. Alvarez-Iglesias, K. Prodromidou, G. Lombardi, L. Frasca, L. P. Berg, and R. I. Lechler. "T cell receptor engagement can influence T cell motility." Transplantation Proceedings 33, no. 1-2 (February 2001): 312–13. http://dx.doi.org/10.1016/s0041-1345(00)02265-x.

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37

Newrzela, S., N. Al-Ghaili, T. Heinrich, M. Petkova, S. Hartmann, B. Rengstl, A. Kumar, et al. "T-cell receptor diversity prevents T-cell lymphoma development." Leukemia 26, no. 12 (May 30, 2012): 2499–507. http://dx.doi.org/10.1038/leu.2012.142.

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38

Yanagi, Yusuke. "T-cell receptor and T-cell-resistant virus variants." Current Opinion in Immunology 3, no. 4 (August 1991): 460–64. http://dx.doi.org/10.1016/0952-7915(91)90003-j.

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39

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 (May 1, 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 the importance of supplementary co-receptors in activation of T helper cells, though little is known about their function in early stage polarization. We hypothesized that the addition of signaling through supplemental co-receptors would alter T helper cell polarization. To conduct these studies, we isolated naïve T cells and polarized them towards Th1 or Tfh fates in the presence or absence of recombinant B7-DC Fc chimera or recombinant B7-H4 Fc chimera. We observed a significant and selective alteration in T helper cell polarization in the presence of these non-canonical co-receptors. These data suggest a complex interplay between cytokine and co-receptor signals that cooperate for robust Th cell polarization. Furthermore, these findings illustrate the potential for novel mechanisms of T cell manipulation for vaccine design and treatment of T cell-mediated diseases.

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40

Grunewald, Johan, Ylva Kaiser, Mahyar Ostadkarampour, Natalia V. Rivera, Francesco Vezzi, Britta Lötstedt, Remi-André Olsen, et al. "T-cell receptor–HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis." European Respiratory Journal 47, no. 3 (November 19, 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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41

Lamers, Cor H. J., Sabine van Steenbergen-Langeveld, Mandy van Brakel, Corrien M. Groot-van Ruijven, Pascal M. M. L. van Elzakker, Brigitte van Krimpen, Stefan Sleijfer, and Reno Debets. "T Cell Receptor-Engineered T Cells to Treat Solid Tumors: T Cell Processing Toward Optimal T Cell Fitness." Human Gene Therapy Methods 25, no. 6 (December 2014): 345–57. http://dx.doi.org/10.1089/hgtb.2014.051.

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Omland, Silje Haukali, Lise Mette Rahbek Gjerdrum, Liszewski Walter, Cerroni L. Lorenzo, and Gniadecki R. Robert. "Primary Cutaneous γδ T-Cell Lymphoma Positive for Both T-Cell Receptor γ and T-Cell Receptor β." Pathology Case Reviews 19, no. 4 (2014): 216–20. http://dx.doi.org/10.1097/pcr.0000000000000047.

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Zhao, Qi. "Novel chimeric antigen receptor T cells based on T-cell receptor-like antibodies." Blood Science 1, no. 2 (October 2019): 144–47. http://dx.doi.org/10.1097/bs9.0000000000000032.

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44

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 (May 1, 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 surface of live primary cells to collect high-dimensional dynamic data for machine learning, which extracts key dynamic features to build predictive diffusion maps. LaMDA spatiotemporally reveals global changes of TCRs across the 3D cell surface, accurately differentiates stimulated cells from unstimulated cells, precisely predicts attenuated T-cell signaling after CD4 and CD28 receptor blockades, and reliably discriminates between structurally similar TCR ligands. We anticipate broad usage of this approach for other receptors and cells, as well as for guiding the design and development of future immunotherapies for cancer, infection, and autoimmunity.

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45

Rodríguez-Jorge, Otoniel, Linda A. Kempis-Calanis, Wassim Abou-Jaoudé, Darely Y. Gutiérrez-Reyna, Céline Hernandez, Oscar Ramirez-Pliego, Morgane Thomas-Chollier, Salvatore Spicuglia, Maria A. Santana, and Denis Thieffry. "Cooperation between T cell receptor and Toll-like receptor 5 signaling for CD4+ T cell activation." Science Signaling 12, no. 577 (April 16, 2019): eaar3641. http://dx.doi.org/10.1126/scisignal.aar3641.

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CD4+ T cells recognize antigens through their T cell receptors (TCRs); however, additional signals involving costimulatory receptors, for example, CD28, are required for proper T cell activation. Alternative costimulatory receptors have been proposed, including members of the Toll-like receptor (TLR) family, such as TLR5 and TLR2. To understand the molecular mechanism underlying a potential costimulatory role for TLR5, we generated detailed molecular maps and logical models for the TCR and TLR5 signaling pathways and a merged model for cross-interactions between the two pathways. Furthermore, we validated the resulting model by analyzing how T cells responded to the activation of these pathways alone or in combination, in terms of the activation of the transcriptional regulators CREB, AP-1 (c-Jun), and NF-κB (p65). Our merged model accurately predicted the experimental results, showing that the activation of TLR5 can play a similar role to that of CD28 activation with respect to AP-1, CREB, and NF-κB activation, thereby providing insights regarding the cross-regulation of these pathways in CD4+ T cells.

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46

Goverman, J. "Chimeric immunoglobulin-T cell receptor proteins form functional receptors: Implications for T cell receptor complex formation and activation." Cell 60, no. 6 (March 23, 1990): 929–39. http://dx.doi.org/10.1016/0092-8674(90)90341-b.

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47

Sarin, A., D. H. Adams, and P. A. Henkart. "Protease inhibitors selectively block T cell receptor-triggered programmed cell death in a murine T cell hybridoma and activated peripheral T cells." Journal of Experimental Medicine 178, no. 5 (November 1, 1993): 1693–700. http://dx.doi.org/10.1084/jem.178.5.1693.

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The hypothesis that cytoplasmic proteases play a functional role in programmed cell death was tested by examining the effect of protease inhibitors on the T cell receptor-mediated death of the 2B4 murine T cell hybridoma and activated T cells. The cysteine protease inhibitors trans-epoxysuccininyl-L-leucylamido-(4-guanidino) butane (E-64) and leupeptin, the calpain selective inhibitor acetyl-leucyl-leucyl-normethional, and the serine protease inhibitors diisopropyl fluorophosphate and phenylmethylsulfonyl fluoride, all showed dose-dependent blocking of the 2B4 death response triggered by the T cell receptor complex and by anti-Thy-1. These protease inhibitors enhanced rather than inhibited IL-2 secretion triggered by T cell receptor cross-linking, showing that they did not act by preventing signal transduction. Growth inhibition induced by cross-linking the 2B4 T cell receptor, measured by inhibition of thymidine incorporation, was not generally blocked by these protease inhibitors. All five of these protease inhibitors enhanced rather than blocked 2B4 cell death triggered by dexamethasone, an agent previously shown to have a death pathway antagonistic with that of the TCR. 2B4 cytolysis by the cytotoxic agents staphylococcal alpha-toxin and dodecyl imidazole, and that caused by hypotonic conditions, was not significantly affected by the five protease inhibitors tested. The selected protease inhibitors blocked both the apoptotic nuclear morphology changes and DNA fragmentation induced by T cell receptor cross-linking, and enhanced both these properties induced by dexamethasone in 2B4 cells. The T cell receptor-induced death of activated murine lymph node T cells and human peripheral blood CD4+ T cells was blocked by both cysteine and serine protease inhibitors, showing that the protease-dependent death pathway also operates in these systems.

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48

Robins, Harlan S., Paulo V. Campregher, Santosh K. Srivastava, Abigail Wacher, Cameron J. Turtle, Orsalem Kahsai, Stanley R. Riddell, Edus H. Warren, and Christopher S. Carlson. "Comprehensive assessment of T-cell receptor β-chain diversity in αβ T cells." Blood 114, no. 19 (November 5, 2009): 4099–107. http://dx.doi.org/10.1182/blood-2009-04-217604.

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Abstract The adaptive immune system uses several strategies to generate a repertoire of T- and B-cell antigen receptors with sufficient diversity to recognize the universe of potential pathogens. In αβ T cells, which primarily recognize peptide antigens presented by major histocompatibility complex molecules, most of this receptor diversity is contained within the third complementarity-determining region (CDR3) of the T-cell receptor (TCR) α and β chains. Although it has been estimated that the adaptive immune system can generate up to 1016 distinct αβ pairs, direct assessment of TCR CDR3 diversity has not proved amenable to standard capillary electrophoresis-based DNA sequencing. We developed a novel experimental and computational approach to measure TCR CDR3 diversity based on single-molecule DNA sequencing, and used this approach to determine the CDR3 sequence in millions of rearranged TCRβ genes from T cells of 2 adults. We find that total TCRβ receptor diversity is at least 4-fold higher than previous estimates, and the diversity in the subset of CD45RO+ antigen-experienced αβ T cells is at least 10-fold higher than previous estimates. These methods should prove valuable for assessment of αβ T-cell repertoire diversity after hematopoietic cell transplantation, in states of congenital or acquired immunodeficiency, and during normal aging.

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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 (May 20, 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). Following pilot experiments to optimize the combined DNA- and RNA-based receptor transfer, the functionality of TETARs was compared to T cells either transfected with the TCR only or the CAR only. After transfection, TETARs clearly expressed both introduced receptors on their cell surface. When stimulated with tumor cells expressing either one of the antigens or both, TETARs were able to secrete cytokines and showed cytotoxicity. The confirmation that two antigen-specific receptors can be functionally combined using two different methods to introduce each receptor into the same T cell opens new possibilities and opportunities in cancer immunotherapy. For further evaluation, the use of these TETARs in appropriate animal models will be the next step towards a potential clinical use in cancer patients.

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Heagy, W., M. Laurance, E. Cohen, and R. Finberg. "Neurohormones regulate T cell function." Journal of Experimental Medicine 171, no. 5 (May 1, 1990): 1625–33. http://dx.doi.org/10.1084/jem.171.5.1625.

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In this communication we show that T cell locomotion is affected by direct interaction with neurohormones. Opioid peptides, including beta-END, MET-ENK, LEU-ENK, and related enkephalin analogues enhanced migration of human peripheral blood T lymphocytes. Activity was dependent on the peptide NH2-terminal sequence, stimulated by enkephalin analogues with specificity for classical delta or mu types of opiate receptor, and inhibited by the opiate receptor antagonist naloxone. Our studies suggest that such neuropeptides stimulate T cell chemotaxis by interaction with sites analogues to classical opiate receptors. We propose that the endogenous opioids beta-END, MET-ENK, and LEU-ENK are potent immunomodulating signals that regulate the trafficking of immune response cells.

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