Relevant bibliographies by topics / TCR

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  2. Dissertations / Theses
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  5. Conference papers
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Academic literature on the topic 'TCR'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 June 2025

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Journal articles on the topic "TCR"

1

Arty, Indyah Sulistyo. "SYNTHESIZE AND CITOTOXICITY TEST OF SEVERAL COMPOUNDS OF MONO PARA-HIDROXY CHALCON." Indonesian Journal of Chemistry 10, no. 1 (June 21, 2010): 110–15. http://dx.doi.org/10.22146/ijc.21489.

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Five compounds of mono para-hidroxy chalcon were synthesized (TC1, TC2, TC3, TC4, and TC5) and tested their cytotoxicity against HeLa cell and Raji cell. The difference in substituent of TC1 (R4 =H), TC2 (R4 = OCH3), and TC3 (R4 = F), showed the difference of their citotoxicity against HeLa cell. The citotoxicity of TC1 (LC50 = 16.08 µg/mL) ≈ TC3 (LC50 = 13.37 µg/mL), but the substituent difference of TC2 (LC50 = 147.43 µg/mL), decreasing it citotoxicity 10 times. Like wise their citotoxicity against Raji cell of TC1 (LC50 = 36.44 µg/mL) ≈ TC3 (LC50 = 30.46 µg/mL), but the substituent difference of TC2 (LC50 = 468.94 µg/mL), decreasing it citotoxicity activity 15 times. Nevertheless the strength of citotoxicity TC4 (LC50 = 98.74 µg/mL) and TC5 (LC50 = 110.97 µg/mL) against Raji cell are stronger than the citotoxicity of two of them against HeLa cell (LC50 of TC4 = none, LC50 of TC5 = 576.53 µg/mL). Keywords: mono para-hidroxy chalcon, HeLa cell, Raji cell, citotoxicity activity
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2

Uruilal, Costanza, Abraham Talahaturuson, Wihelmina Rumahlewang, and Jogeneis Patty. "ISOLASI Trichoderma spp. DAN DAYA ANTAGONISMENYA TERHADAP SCLEROTIUM ROLFSII SACC. PENYEBAB PENYAKIT LAYU PADA TANAMAN CABAI (Capsicum anuum) SECARA IN-VITRO." JURNAL BUDIDAYA PERTANIAN 13, no. 2 (December 1, 2017): 64–67. http://dx.doi.org/10.30598/jbdp.2017.13.2.64.

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The objective of this study is to isolation and agonistic test ability of Trichoderma spp. againts Sclerotium rolfsii Sacc. cause of wilting on pepper plants and has been conducted in Pathogenicity Laboratory Faculty of Agriculture Unpatti. The study use 5 treatment of isolate Trichoderma spp. (Tc3, Tc4, Tc5, Tc6 and Tc7) with 3 replications so that there are 15 experimental units. The results showed that the five isolates Trichoderma spp. has an antagonistic power to S. rolfsii with an average percentage of inhibition of S. rolfsii of 26,01%. Percentage of inhibition bolth of isolate ware not significantly different at 95% level test results between treatment. Average percentage inhibition of S. rolfsii by Trichoderma spp. each treatment was Tc6 = 27,31%, Tc3 = 26,63%, Tc5 = 26,05%, Tc7 = 25,69% and Tc4 = 24,37%.
 Keywords: antagonism, Trichoderma spp., Sclerotium rolfsii
 
 Abstrak
 Penelitian ini bertujuan mengisolasi dan menguji kemampuan antagonis Trichoderma spp. terhadap Sclerotium rolfsii Sacc. penyebab layu pada tanaman cabai dan telah dilaksanakan di Laboratorium Patogenisitas Fakultas Pertanian Unpatti, dengan menggunakan 5 perlakuan isolat Trichoderma spp. (Tc3, Tc4, Tc5, Tc6 dan Tc7) dengan 3 ulangan sehingga terdapat 15 satuan percobaan. Hasil penelitian menunjukkan bahwa kelima isolat Trichoderma sp. mempunyai daya antagonis terhadap S. rolfsii dengan rata-rata persentase penghambatan S. rolfsii sebesar 26%. Hasil analisis varians pada taraf 95% menunjukkan tidak ada perbedaan nyata antara perlakuan. Rata-rata persentase penghambatan S. rolfsii oleh Trichoderma spp. masing-masing perlakuan berturut-turut adalah Tc6 = 27,31%, Tc3 = 26,63%, Tc5 = 26,05%, Tc7 = 25,69% dan Tc4 = 24,37%, dengan rata-rata 26,01%.
 Kata kunci: antagonisme, Trichoderma spp., Sclerotium rolfsii
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3

Bagot, Martine, Hamid Echchakir, Fathia Mami-Chouaib, Marie-Hélène Delfau-Larue, Dominique Charue, Alain Bernheim, Salem Chouaib, Laurence Boumsell, and Armand Bensussan. "Isolation of Tumor-Specific Cytotoxic CD4+ and CD4+CD8dim+ T-Cell Clones Infiltrating a Cutaneous T-Cell Lymphoma." Blood 91, no. 11 (June 1, 1998): 4331–41. http://dx.doi.org/10.1182/blood.v91.11.4331.

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Abstract We have isolated several T-cell clones from lymphocytes infiltrating a human major histocompatibility class (MHC) II negative cutaneous T-cell lymphoma (CTCL). We describe here two of these clones, TC5 and TC7, with, respectively, a CD4+CD8dim+ and CD4+CD8− phenotype. Both clones mediated a specific MHC class I–restricted cytotoxic activity toward the fresh autologous tumor cells, and autologous tumor cell lines previously established with interleukin-2 (IL-2) and IL-7 from the skin and from the blood. Analysis of the T-cell receptor (TCR) Vβ gene expression showed that the tumor cells, which were shown to have a trisomy 7 by fluorescent in situ hybridization, expressed Vβ7/Jβ2.3, Vβ13/Jβ2.5, and Vβ22/Jβ2.5 rearrangements. Phenotypic analysis using specific anti-Vβ monoclonal antibodies indicated that only Vβ13 could be detected on the cell membrane of the tumor cells. Analysis of the TCR Vβ gene expression of the clones showed that TC5 and TC7 expressed a unique TCR-Vβ transcript, corresponding, respectively, to Vβ5/Jβ2.3 and Vβ17/Jβ2.7 gene segments. To determine whether these reactive T lymphocytes were present in vivo, we used specific primers corresponding to TC5- and TC7-Vβ TCR transcripts. The results showed that both cytotoxic T-cell clones were present at the lesional skin site and amplified in vitro. TC7 was found in the patient peripheral blood invaded by tumoral cells, whereas TC5 was not, indicating that the repertoire of the reactional lymphocytes differs in the blood and at the tumor site. These results show for the first time the presence of reactive T lymphocytes with CD4 or double-positive phenotype infiltrating a CTCL. These findings raise the question of the role of these antitumoral effector T cells in the tumor growth.
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4

Bagot, Martine, Hamid Echchakir, Fathia Mami-Chouaib, Marie-Hélène Delfau-Larue, Dominique Charue, Alain Bernheim, Salem Chouaib, Laurence Boumsell, and Armand Bensussan. "Isolation of Tumor-Specific Cytotoxic CD4+ and CD4+CD8dim+ T-Cell Clones Infiltrating a Cutaneous T-Cell Lymphoma." Blood 91, no. 11 (June 1, 1998): 4331–41. http://dx.doi.org/10.1182/blood.v91.11.4331.411k12_4331_4341.

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We have isolated several T-cell clones from lymphocytes infiltrating a human major histocompatibility class (MHC) II negative cutaneous T-cell lymphoma (CTCL). We describe here two of these clones, TC5 and TC7, with, respectively, a CD4+CD8dim+ and CD4+CD8− phenotype. Both clones mediated a specific MHC class I–restricted cytotoxic activity toward the fresh autologous tumor cells, and autologous tumor cell lines previously established with interleukin-2 (IL-2) and IL-7 from the skin and from the blood. Analysis of the T-cell receptor (TCR) Vβ gene expression showed that the tumor cells, which were shown to have a trisomy 7 by fluorescent in situ hybridization, expressed Vβ7/Jβ2.3, Vβ13/Jβ2.5, and Vβ22/Jβ2.5 rearrangements. Phenotypic analysis using specific anti-Vβ monoclonal antibodies indicated that only Vβ13 could be detected on the cell membrane of the tumor cells. Analysis of the TCR Vβ gene expression of the clones showed that TC5 and TC7 expressed a unique TCR-Vβ transcript, corresponding, respectively, to Vβ5/Jβ2.3 and Vβ17/Jβ2.7 gene segments. To determine whether these reactive T lymphocytes were present in vivo, we used specific primers corresponding to TC5- and TC7-Vβ TCR transcripts. The results showed that both cytotoxic T-cell clones were present at the lesional skin site and amplified in vitro. TC7 was found in the patient peripheral blood invaded by tumoral cells, whereas TC5 was not, indicating that the repertoire of the reactional lymphocytes differs in the blood and at the tumor site. These results show for the first time the presence of reactive T lymphocytes with CD4 or double-positive phenotype infiltrating a CTCL. These findings raise the question of the role of these antitumoral effector T cells in the tumor growth.
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5

Goux, Delphine, Jérôme D. Coudert, Diane Maurice, Leonardo Scarpellino, Grégoire Jeannet, Stefano Piccolo, Kathleen Weston, Joerg Huelsken, and Werner Held. "Cooperating pre–T-cell receptor and TCF-1–dependent signals ensure thymocyte survival." Blood 106, no. 5 (September 1, 2005): 1726–33. http://dx.doi.org/10.1182/blood-2005-01-0337.

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Abstract Intrathymic T-cell maturation critically depends on the selective expansion of thymocytes expressing a functionally rearranged T-cell receptor (TCR) β chain. In addition, TCR-independent signals also contribute to normal T-cell development. It is unclear whether and how signals from the 2 types of pathways are integrated. Here, we show that T-cell factor-1 (TCF-1), a nuclear effector of the canonical wingless/int (wnt)/catenin signaling pathway, ensures the survival of proliferating, pre-TCR+ thymocytes. The survival of pre-TCR+ thymocytes requires the presence of the N-terminal catenin-binding domain in TCF-1. This domain can bind the transcriptional coactivator β-catenin and may also bind γ-catenin (plakoglobin). However, in the absence of γ-catenin, T-cell development is normal, supporting a role for β-catenin. Signaling competent β-catenin is present prior to and thus arises independently from pre-TCR signaling and does not substantially increase on pre-TCR signaling. In contrast, pre-TCR signaling significantly induces TCF-1 expression. This coincides with the activation of a wnt/catenin/TCF reporter transgene in vivo. Collectively, these data suggest that efficient TCF-dependent transcription requires that pre-TCR signaling induces TCF-1 expression, whereas wnt signals may provide the coactivator such as β-catenin. The 2 pathways thus have to cooperate to ensure thymocyte survival at the pre-TCR stage. (Blood. 2005;106:1726-1733)
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6

Ciurea, Stefan O., Rima M. Saliba, Ulas D. Bayraktar, Susan Xie, Gabriela Rondon, Simrit Parmar, Partow Kebriaei, et al. "Improved Early Outcomes with T-Cell Replete (TCR) Compared with T-Cell Depleted (TCD) Haploidentical Stem Cell Transplantation (HaploSCT)." Blood 118, no. 21 (November 18, 2011): 320. http://dx.doi.org/10.1182/blood.v118.21.320.320.

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Abstract Abstract 320 Background: HaploSCT has been commonly performed with a TCD graft using CD34+ selection; however, this has been limited by a higher non-relapse mortality (NRM) primarily related to infectious complications. An alternative approach using a TCR bone marrow graft and high-dose post-transplant cyclophosphamide (HDPTCy) in the setting of non-myeloablative conditioning has been reported to have lower NRM and acceptable rates of GVHD. Methods: We hypothesized that TCR HaploSCT using HDPTCy is associated with improved immunologic reconstitution, less NRM and better early outcomes compared with TCD HaploSCT, and analyzed 65 consecutive patients (pts) treated at UTMDACC with the same conditioning regimen, fludarabine (40mg/m2/day × 4), melphalan (140mg/m2) and thiotepa (10mg/kg). TCD HaploSCT pts were treated between 2001 and 2009, while TCR patients after 2009. 6 pts in the TCR group >55 years/comorbidities received reduced doses of melphalan (100mg/m2) and thiotepa (5mg/kg). There was no GVHD prophylaxis in the TCD group, while TCR group received HDPTCy (50mg/kg/day × 2) followed by tacrolimus and mycophenolate. Results: The median follow-up was 10 months (range 3.5–25) for the TCR group and 44 (11–79) months for the TCD group. Median age was 45 years (range 20–63) in the TCR group and 36 years (range 18–56) in the TCD group (p=0.02). 28% were > 50 years in the TCR compared with 6% in the TCD group (p=0.02). Diagnoses were: AML/MDS 50% vs. 79%, ALL 13% vs. 12%, CML 16% vs. 6%, lymphoma/CLL 9% vs. 3% in the TCR vs. TCD groups, respectively. Only 13 (41%) and 12 (36%) of pts were in remission at transplant in both groups, respectively (p=0.7). 10/16 (62.5%) pts with AML/MDS in the TCR group had poor risk cytogenetics vs. 13/26 (50%) pts in the TCD group. The donors were 5/10 allele match in 20/32 (63%) and 16/31 (52%) in the two groups, respectively. Median numbers of CD34+ cells infused were 2.5×10e6/kg in the TCR group and 10.5×10e6/kg in the TCD group. All pts in the TCD group had peripheral blood selected CD34+ cells while all but one received bone marrow stem cells in the TCR group. One pt had early death in each group. Primary engraftment was achieved in 94% in the TCR group and 81% in the TCD group (p=0.1). Day-100 NRM for all pts was 9% in the TCR group vs. 21% for the TCD group, and for pts in remission at transplant 0% vs. 42%, respectively (p=0.01). NRM at 1 year for all pts was 16% for the TCR group vs. 42% for the TCD group (p=0.03) (Figure1), while for pts in remission was 0% vs. 67% (p=0.001). The cumulative incidences of grade II-IV aGVHD was 27% vs. 11% (p=0.5) and cGVHD was 8% vs. 18%, in the TCR and TCD group, respectively (p=0.03). OS and PFS at 1 year post-transplant were 66% vs. 30% (p=0.02) and 45% vs. 21% (p=0.03) for the whole group, and 92% vs. 33% (p=0.03) and 80% vs. 25% (p=0.02) for pts in remission at transplant, respectively (Figure1). Improved NRM in the TCR group was related to significantly better immunologic reconstitution of T-cell subsets. On day 30 post transplant there was a significantly better recovery of absolute CD4 cells in the TCR group (median 24 vs. 2, p=0.004) and CD8 cells (median 20.5 vs. 1.5, p=0.036). CD4 cells remained significantly lower in the TCD group until after day 180 when the median CD4 count was 200.5 vs. 64 in the TCR group (p=0.04) while the difference in CD8 counts became non-significantly higher in the TCR after day 90 (median 119 vs. 29, p=0.23). Conclusion: TCR HaploSCT is associated with better immunologic reconstitution and improved early outcomes compared with TCD HaploSCT. Disclosures: No relevant conflicts of interest to declare.
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Delea, Thomas, Aaron Moynahan, Wenzhen Ge, Xue Song, Glenn S. Kroog, Irene Noguera-Troise, Karen Rodriguez Lorenc, and Qiufei Ma. "Real-World Study of Patients with Triple-Class Exposed Relapsed/Refractory Multiple Myeloma: Analysis across a Spectrum of Advanced Disease Stage Medicare Patients in the United States." Blood 142, Supplement 1 (November 28, 2023): 3773. http://dx.doi.org/10.1182/blood-2023-188591.

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Background Treatment of relapsed/refractory (RR) multiple myeloma (MM) has been transformed by novel therapies including anti-CD38 monoclonal antibodies (mAb), 2 nd and 3 rd generation immunomodulatory drugs (IMiD), and proteasome inhibitors (PI). This has resulted in increasing numbers (no.) of triple-class exposed (TCE) patients (pts), defined as pts who have received an IMiD, ≥1 PI, and ≥1 anti-CD38 mAb. Many TCE pts are exposed to ≥5 drugs in these classes (i.e. penta-exposed [PE]: ≥2 IMID, ≥2 PI, and an anti-CD38 mAb). Some are refractory to ≥1 drug in each class (triple-class refractory [TCR]) and some are both PE and TCR (PE-TCR). Data on real-world outcomes for the spectrum of heavily pre-treated, advanced RRMM pts are limited. This study examined treatment patterns and healthcare resource utilization (HRU) and costs in Medicare-insured pts with TCE RRMM. Methods Adult pts with an incident diagnosis (Dx) of MM (≥2 outpatient claims 30-365 days apart OR ≥1 inpatient AND 6 months [mos.] of continuous eligibility prior to first Dx) during the study period (Nov 14, 2006-Dec 31, 2020) who were TCE were selected from the Center for Medicare and Medicaid Services Chronic Conditions Data Warehouse. TCE was defined as having ≥1 claim each for an IMiD, a PI, and an anti-CD38 mAb; PE was defined as having ≥2 claims each for an IMiD and a PI and ≥1 claim for an anti-CD38 mAb (TCE pts were assumed to have RRMM based on exposure). Pts were deemed TCR if refractory to ≥1 regimen each which included a PI, an IMiD, and an anti-CD38 mAb. Pts were considered refractory to a regimen if the period between the last claim or days supplied for any drug in the regimen and the start of the subsequent regimen was <60 days AND none of the drugs in the regimen were present in the next regimen. For each pt, the 1 st line of therapy (LOT) after becoming TCE was considered the index LOT and the date that this LOT initiated was defined as the index date. Pts were followed from the index date until the earliest of end of continuous enrollment or the end of study period. LOTs and treatment regimens were defined using an adaptation of published algorithm developed based on clinical expert opinion (Madduri et al. Future Oncol. 2021). Outcomes included anti-MM treatments received for index LOT, time to discontinuation (TTD), time to next treatment (TTNT), overall survival (OS), and post-index HRU and healthcare costs (adjusted to 2021 USD). Median TTD and OS were obtained by Kaplan-Meier (KM) methods. TTNT was analyzed by cumulative incidence methods with death as a competing risk. HRU and costs (in 2021 USD) were reported on a per patient per month (PPPM) basis. Results 137,707 pts with an MM Dx during the study period were identified. A total of 2,830 TCE, 1,371 TCR, 1,121 PE, and 774 PE-TCR pts met all other inclusion criteria. Mean age was 76 years in all 4 cohorts, 50-51% were female, 21% (TCR) to 29% (PE) had prior autologous stem cell transplant. The mean no. of prior LOTs ranged from 3.3 (TCE) to 4.5 (PE-TCR). The no. of new TCE pts increased almost 8-fold from 114 in 2016 to 890 in 2020; similar increases were observed for TCR, PE, and PE-TCR pts. Mean (SD) follow-up time (mos.) was 12.4 (10.6) for TCE, 11.9 (10.0) for TCR, 10.9 (10.3) for PE, and 10.1 (9.3) for PE-TCR. There was no apparent standard of care (SOC) treatment across the 4 cohorts; the most frequently used index LOT regimens were pomalidomide + daratumumab for TCE (17%) and PE (7%), pomalidomide + carfilzomib for TCR (10.3%), and pomalidomide + elotuzumab for PE-TCR (7.4%). In all 4 cohorts, pomalidomide was the most frequently received medication during the index LOT (32.6% [PE-TCR] to 43.3% [TCR]). Median TTD (mos.) ranged from 4.2 (PE-TCR) to 6.9 (TCE). Median TTNT (mos.) ranged from 8.1 (TCR) to 14.6 (TCE). Median OS (mos.) ranged from 13.0 (TCR) to 15.9 (PE). TCE pts had a mean PPPM 0.20 ED visits, 7.02 outpatient visits, 3.73 outpatient pharmacy claims, 0.14 hospitalizations, and 1.18 inpatient days. For TCE pts, mean PPPM total costs were $23,091, the largest share of which was for MM medications ($16,812), followed by other MM-related services ($4,824). Monthly HRU and costs for TCR, PE, and PE-TCR pts were similar to those for TCE. Conclusions Despite increasing no. of Medicare-insured TCE, TCR, PE, and PE-TCR MM pts, there is no apparent SOC treatment regimen. With current treatments, TTD, TTNT, and OS are short and HRU and costs are high. These data underscore the high unmet need for new therapies in this growing population.
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Sun, Hanli, Jiao Huang, Kai Zhan, Wanli Wu, Xianqing Tang, Min Liu, Shanshan Guo, Hongjun Zheng, Yingjie Huang, and Shi Zhong. "Abstract 3598: A new strategy for T cell therapy: T cells secreting TCR anti-CD3 bispecific T-cell engager." Cancer Research 84, no. 6_Supplement (March 22, 2024): 3598. http://dx.doi.org/10.1158/1538-7445.am2024-3598.

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Abstract TCR-engineered T (TCR-T) cells and TCR-anti-CD3 bispecific T-cell engagers (TCEs) are potent TCR-based therapeutic agents with distinct advantages and limitations in tumor treatment. TCR-T cells offer durable persistence within patients but necessitate personalized manufacturing and lack the capacity to harness bystander T cells. Conversely, TCEs are readily available as "off-the-shelf" products and can recruit bystander T cells, yet they exhibit a shorter lifespan. In our study, we sought to merge the merits of both approaches by engineering T cells to secrete a TCR-anti-CD3 TCE specific for alpha fetoprotein (AFP), a tumor-associated antigen abundantly expressed in hepatocellular carcinoma (HCC). We initially identified a TCR with specificity for the AFP158-166 peptide bound to HLA-A*02:01 and enhanced its affinity to picomolar via phage display. To facilitate efficient secretion by T cells, we adapted the high-affinity TCR to a single-chain format (scTCR) and fused it with a CD3-specific single-chain antibody fragment (scAFP-TCE). Our findings demonstrated that scAFP-TCE effectively redirected bystander T cells to engage in the lysis of HCC cells. Moreover, scAFP-TCE could be secreted by T cells transduced with lentiviral particles encoding the TCE gene. These transduced T cells exhibited potent antitumor activity both independently and by enlisting bystander T cells. This innovative T cell strategy, combining the bystander-recruiting ability of fusion proteins with the durable persistence seen in T cell therapy after a single infusion, presents a promising alternative to conventional TCR-based therapeutic agents. We anticipate that this novel approach may hold substantial potential for enhancing HCC treatment and expanding the scope of TCR-based immunotherapies. Citation Format: Hanli Sun, Jiao Huang, Kai Zhan, Wanli Wu, Xianqing Tang, Min Liu, Shanshan Guo, Hongjun Zheng, Yingjie Huang, Shi Zhong. A new strategy for T cell therapy: T cells secreting TCR anti-CD3 bispecific T-cell engager [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3598.
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Abdulazim, Amr, Nora Prochnow, and Tara Taeihagh. "TCR or Not TCR?" Journal of Oral and Maxillofacial Surgery 69, no. 10 (October 2011): 2483–84. http://dx.doi.org/10.1016/j.joms.2011.05.028.

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Oros-Ortega, Iván, Alejandro Alonso-López, Jesús Pérez-Moreno, Jorge C. López-Collado, Luis A. Lara-Pérez, Sandra E. Martínez-Garza, Laura Y. Solís-Ramos, and Antonio Andrade-Torres. "Respuesta de plántulas de Cedrela odorata a la inoculación con Rhizophagus intraradices y diferentes niveles de defoliación." Revista Mexicana de Ciencias Agrícolas 6, no. 3 (December 8, 2017): 627. http://dx.doi.org/10.29312/remexca.v6i3.645.

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 Respuesta de plántulas de Cedrela odorata a la inoculación con Rhizophagus intraradices y diferentes niveles de defoliación ; el efecto de seis tratamientos (T) sobre la tasa de crecimiento en altura (TCA) , diámetro ( TCD ) , tasa de crecimiento relativo (TCR ) y peso fresco y seco de plántulas de C. odorata se evaluaron en un vivero. Se utilizó un diseño completamente al azar con arreglo factorial (2 x 3); TS consistió en una combinación de los factores: porcentaje de defoliación (0, 50 y 90) y la inoculación de R. intraradices (con y sin inoculación). Después de seis meses, las plántulas de TS con la inoculación, independientemente del porcentaje de defoliación aplicada, mostraron más TCD (F= 100.45, p< 0,001) que TS sin inoculación. Las TS inoculadas, con diferentes niveles de defoliación, mostró el mayor TCA (F= 556.57 p< 0,001) después de tres meses. Sin embargo los últimos tres meses la interacción de la inoculación/ defoliación (50 y 90 %) indujo el mayor valor de TCA (F= 4.22 p< 0.01), y un crecimiento significativo en el peso fresco y seco de tallos, hojas y raíces. La inoculación produce altos niveles de micorrización en las raíces de C. odorata en el sexto mes. La defoliación al 90 % reduce significativamente la colonización de hifas y vesículas. Durante los tres primeros meses, las TS inoculadas mostraron el valor más alto de TCR, sin embargo, en los últimos tres meses los tratamientos sin inoculación y defoliación al 90% presentaron la mayor TCR. La interacción Inoculación / defoliación tiene efectos en el desarrollo de C. odorata, por lo que es conveniente considerar este tratamiento para la producción de plántulas en vivero.
 
 
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Dissertations / Theses on the topic "TCR"

1

Groves, Tim C. "Pre-TCR and TCR-Ãß signaling during T cell development." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ27657.pdf.

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Currie, James. "Stochastic modelling of TCR binding." Thesis, University of Leeds, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590430.

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A fundamental process in the immune response to infection is the activation of T cells following contact with antigen presenting cells. This activation occurs after T cell receptors on the surface of T cells bind to immunogenic peptides expressed on the surface of antigen presenting cells. The binding of T cell receptors to ligands not only leads to the activation of T cells, it is also key to T cell selection in the thymus and the maintenance of a diverse T cell receptor repertoire. T cell receptor bindings are converted into a signal which activates a T cell but there is no universal theory which governs this process. There is experimental evidence to suggest that receptor-ligand bindings must be sufficiently long to elicit a T cell response. and that counting devices in the T cell work to allow signal accumulation, decoding and translation into biological responses. In view of these results, this thesis uses mathematical models to explore the timescales associated with T cell responses. A stochastic criterion that T cell responses occur after N receptor-ligand complexes have been bound for at least a dwell time, T, each, is used. The first model of receptor-ligand binding, in conjunction with the stochastic criterion, supports the affinity threshold hypothesis for thymic selection and agrees with the experimentally established ligand hierarchy for thymic negative selection. The initial model of ligand-receptor binding is then extended to include feedback responses, bivalent receptor binding and ligand diffusion through the immunological synapse. By including these mechanisms, the models agree with an array of experimental hypotheses which include: T cells exhibit a digital response to ligand. bivalent T cell receptor engagement stabilises receptor-ligand bindings and one ligand is sufficient to elicit a T cell response.
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Lacroix, France. "T cell receptor (TCR) for antigen: A comparative study between the TCR alpha/beta and TCR gamma/delta subsets in noninfected and HIV infected individuals." Thesis, University of Ottawa (Canada), 1993. http://hdl.handle.net/10393/6937.

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HIV infection is associated with characteristic quantitative changes in T-lymphocyte subsets: progressive depletion of the CD4$\sp{+}$ T-lymphocytes and an increased number of the CD8$\sp{+}$ T-lymphocyte. In this study, I report the results of a flow cytometric analysis of the expression of CD3, CD4, CD8, TCR$\alpha$/$\beta$, and TCR$\gamma$/$\delta$ antigens. I observed that CD8$\sp{+}$TCR$\alpha$/$\beta\sp{+}$ cells increased early in HIV disease (p 0.01) whereas the frequency of CD4$\sp{+}$TCR$\alpha$/$\beta\sp{+}$ cells was relatively unchanged. The frequency of TCR$\gamma$/$\delta\sp{+}$ cells remained unchanged. However, the mean fluorescence intensity (MFI), reflecting surface antigenic density, varied and allowed a clear distinction among different stages of infection. The expression of three activation markers (HLA-DR, CD38, CD57) was clearly increased in HIV infected individuals. The TCR$\alpha$/$\beta$ subset showed more substantial variation for activation markers. In the TCR$\gamma$/$\delta$ subset, the CD57 antigen seemed to be the most affected by the state of the disease and showed the greatest increase (p 0.01). (Abstract shortened by UMI.)
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Mariathasan, Sanjeev. "TCR-mediated signaling in thymocyte selection." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63683.pdf.

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Rivera, Reyes Brenda Mariola. "Regulation of the TCR signaling pathway." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1132588714.

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Barry, A. C. "Regulation of TCR signalling by SOCS." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479241.

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Mallaun, Michel. "Proximal TCR signaling in self tolerance /." [S.l.] : [s.n.], 2008. http://edoc.unibas.ch/diss/DissB_8729.

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Huang, Elizabeth Chi-Fang. "Organisation of, and ligand-independent signalling by, the TCR, with a special emphasis on the pre-TCR." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:0c01e3d4-2002-487c-a0b6-09ed20cb223b.

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Understanding how immune signalling is initiated and regulated spatiotemporally is likely to be helped by investigations of receptor stoichiometry. The pre-TCR expressed by thymocytes shares similarities in structure and signalling components with the mature TCR but, in contrast to the TCR, it has no known ligands. This thesis has therefore analysed the stoichiometry of the pre-TCR using mutagenesis- and imaging-based approaches, and explored how ligand-independent signalling might be initiated by both the TCR and pre-TCR. The mutational analysis, which required considerable optimisation because the pre-TCR is very weakly expressed in transfected cells, suggested that only one contiguous surface on pre-Tα needs to be buried in the pre-TCR complex in order for it to reach the cell surface. This comprised the surface buried at the interface with the constant region of TCRβ and therefore was incompatible with previous suggestions that the pre-TCR assembles into a 'head-to-tail' dimer. Unexpectedly, super-resolution imaging experiments combined with cluster analysis, and the method of single-molecule cross-colour coincidence detection were suggestive that, rather than dimers, the pre-TCR forms higher-order oligomers in transfected cells and possibly also in thymocytes. Similar analyses showed that the organisation of the TCR was heterogeneous, depending on the level of expression of the receptor. Overall, technical limitations that emerged in the course of the study highlighted some of the difficulties in studying native receptor stoichiometry on resting cells generally. The final part of the thesis investigated ligand-independent signalling by the TCR, using a novel assay based on the binding of a superagonistic antibody to a non-signalling form of the receptor CD28. Using CRISPR/Cas-mediated gene editing, it was shown that ligand-independent signalling by the mature TCR and pre-TCR was dependent on Lck and Zap70, indicating that it is reliant on the triggering of conventional signalling pathways. Ways in which the pre-TCR might initiate signalling, that could be tolerant of complexes exhibiting a range of stabilities, are also discussed.
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Bunse, Mario. "RNAi-mediated knockdown of the endogenous TCR improves safety of immunotherapy with TCR gene-modified T cells." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17155.

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Durch den Transfer der Gene des heterodimeren T-Zellrezeptors (TZR) mithilfe viraler Vektoren können T-Zellen programmiert werden, ein ausgewähltes Antigen spezifisch zu erkennen. In klinischen Studien wurden solche T-Zellen bereits mit Erfolg zur Immuntherapie von Krebs und viralen Infektionen eingesetzt. Genmodifizierte T-Zellen unterscheiden sich jedoch von normalen T-Zellen, weil sie neben den beiden zelleigenen auch die zwei übertragenen TZR-Gene exprimieren. Diese Situation erlaubt die Bildung vier verschiedener TZR-Heterodimere: der zelleigene TZR, der übertragene TZR und zwei gemischte TZR, bestehend aus je einer übertragenen und einer zelleigenen TZR-Kette. Gemischte TZR bergen das Risiko von Nebenwirkungen, weil sie durch Zufall gesundes Körpergewebe erkennen und so Autoimmunität auslösen könnten. In dieser Arbeit wurden deshalb virale Vektoren entwickelt, die gleichzeitig mit der Übertragung von neuen TZR-Genen den zelleigenen TZR durch RNA Interferenz (RNAi) unterdrücken. Mikro-RNA (miRNA), die in den Vektor MP71 eingefügt wurden, reduzierten den zelleigenen TZR in Maus-T-Zellen um mehr als 85%. Dies hatte zur Folge, dass beide Ketten des übertragenen P14-TZR in gleicher Menge auf der Zelloberfläche exprimiert wurden und die Bildung von gemischten TZR reduziert wurde. In einem Mausmodell der adoptiven T-Zelltherapie verhinderte die Unterdrückung des zelleigenen TZR die Entstehung von Autoimmunität, die andernfalls durch gemischte TZR verursacht wurde. Im Gegensatz dazu führte die Anwendung von gentechnisch optimierten P14-TZR-Genen weder zur angeglichenen Oberflächenexpression der P14-TZR Ketten noch zu weniger Autoimmunität im Mausmodell. Ein anderes Tierexperiment zeigte, dass die miRNA die Funktion der genmodifizierten T-Zellen nicht beeinträchtigte. Schließlich wurde ein viraler Vektor entwickelt und getestet, der die Expression des zelleigenen TZR in menschlichen T-Zellen effektiv unterdrückte und die Bildung von gemischten TZR reduzieren konnte.<br>T cells can be genetically modified using viral vectors. The transfer of genes encoding both chains of the heterodimeric T cell receptor (TCR) programs T cells to specifically react towards an antigen of choice. Such TCR gene-modified T cells were already successfully applied in clinical studies to treat cancer and viral infections. However, in contrast to nonmanipulated T cells these cells express the transferred TCR in addition to the endogenous TCR and this situation allows the assembly of four different TCR heterodimers: the endogenous TCR, the transferred TCR, and two mixed TCR dimers, composed of one endogenous and one transferred TCR chain. The formation of mixed TCR dimers represents a safety issue because they may by chance recognize self-antigens and thereby cause autoimmune side effects. To overcome this problem, an RNAi-TCR replacement vector was developed that simultaneously silences the endogenous TCR and expresses an RNAi-resistant therapeutic TCR. The expression of miRNA encoded by a retroviral MP71 vector in transduced mouse T cells reduced the surface levels of the endogenous TCR by more than 85%. The knockdown of the endogenous TCR in turn resulted in equal surface expression levels of both transferred P14 TCR chains and prevented the formation of mixed TCR dimers. Accordingly, the development of lethal mixed TCR dimer-dependent autoimmunity (TI-GVHD) in a mouse model of adoptive T cell therapy was dramatically reduced by the knockdown of the endogenous TCR. In contrast, the usage of genetically optimized TCR genes neither resulted in equal surface levels of both P14 TCR chains nor in reduced autoimmunity. A second mouse model demonstrated that the in vivo functionality of the transduced T cells was not negatively influenced by the expression of the miRNA. Finally, an RNAi-TCR replacement vector for human T cells was developed that effectively reduced the expression of the endogenous TCR and prevented the formation of mixed TCR dimers.
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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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Books on the topic "TCR"

1

T, Petrie Howard, ed. Non-TCR-mediated mechanisms of thymocyte differentiation. London: Academic Press, 2000.

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T, Petrie Howard, ed. Non-TCR-mediated mechanisms of thymocyte differentiation. London: Academic Press, 2000.

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Ruffi, Lapo. Lapo Ruffi, Edificio TCR: Pistoia, Italy, 2008-2009. Poggibonsi (SI) [i.e. Siena, Italy]: Forma, 2011.

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Groves, Tim C. Pre-TCR and TCRab signaling during T cell development. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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Hammad, Nazik. A transgenic TCR model for studying the veto phenomenon. Ottawa: National Library of Canada, 1994.

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Bi, Yunchen. Study of the Calcium Regulation Mechanism of TCR Activation Using Nanodisc and NMR Technologies. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-54618-5.

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Cheng, Gordon W. Functions of CD45 in TCR signaling in CD4p+sCD8p+s double-positive thymocytes. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Ford, Megan. The role and mechanism of B6/1pr TCR[alpha beta]+CD4-CD8- T cells in immune response regulation. Ottawa: National Library of Canada, 2001.

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Galley, Kevin Andrew. Analysis of junctional region diversity of TCR[beta] cDNA from pancreatic islet-infiltrating T cells of young prediabetic nonobese diabetic mice. Ottawa: National Library of Canada, 1994.

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Korpela, Mikko. Organizational Information Systems in the Context of Globalization: IFIP TC8 & TC9. Boston, MA: Springer US, 2003.

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Book chapters on the topic "TCR"

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Maeurer, Markus J. "TCR Analyses." In Analyzing T Cell Responses, 239–60. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3623-x_14.

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Jameson, Stephen C., and Kristin A. Hogquist. "Options for TCR Interactions: TCR Agonists, Antagonists and Partial Agonists." In MHC Molecules: Expression, Assembly and Function, 181–90. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_11.

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Vandenbark, Arthur A., George Hashim, and Halina Offner. "TCR Peptide Therapy in Autoimmunity." In Progress in Immunology Vol. VIII, 635–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_82.

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Rhein, Simone, and Neşe Çakmak-Görür. "TCR Gene Therapy for Cancer." In Methods in Molecular Biology, 95–128. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2441-8_6.

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Peruzzi, Benedetta, Sara Bencini, and Roberto Caporale. "TCR Vβ Evaluation by Flow Cytometry." In Methods in Molecular Biology, 99–109. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1311-5_8.

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Venu, Y., T. Nireekshana, B. Phanisaikrishna, Ramavath Gnanendar, and S. Ravikumar. "Reducing TCR Harmonics Using Sequential Switching." In Advances in Automation, Signal Processing, Instrumentation, and Control, 2503–10. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-8221-9_233.

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Porcelli, S., P. A. Bleicher, J. L. Greenstein, S. P. Balk, C. Terhorst, and M. B. Brenner. "Lymphocytes Bearing Either γδ-TCR or αβ-TCR Can Recognize Non-MHC Encoded CD1 Molecules." In Progress in Immunology, 29–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_5.

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Yamaguchi, Rui, Seiya Imoto, and Satoru Miyano. "A TCR Sequence Data Analysis Pipeline: Tcrip." In Immunopharmacogenomics, 27–43. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55726-5_2.

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Gervois, Nadine, Bing-Yuan Wei, Paolo Dellabona, Jean Peccoud, Christophe Benoist, and Diane Mathis. "Structure of the TCR-Ag-MHC Complex." In T Lymphocytes, 17–23. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_2.

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Neagu, Monica, and Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases." In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.

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AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.
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Conference papers on the topic "TCR"

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Myrick, Wilbur, Nobuyasu Shiga, Julian St James, and Ahmad Byagowi. "Timing, Communications, and Ranging SDR (TCR-SDR) for IoT Wireless Synchronization." In 2024 IEEE International Symposium on Precision Clock Synchronization for Measurement, Control, and Communication (ISPCS), 1–7. IEEE, 2024. http://dx.doi.org/10.1109/ispcs63021.2024.10747731.

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Wang, Haoyan, Yuhang Yang, Yifei Huang, Tianyi Zang, and Yadong Liu. "TDLM: A Diffusion Language Model for TCR Sequence Exploration and Generation." In 2024 IEEE International Conference on Bioinformatics and Biomedicine (BIBM), 113–20. IEEE, 2024. https://doi.org/10.1109/bibm62325.2024.10821797.

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Andrews, Sean. "Staring at the sun: advanced TCR materials for robust thermal imaging." In Infrared Technology and Applications LI, edited by David Z. Ting, Gabor F. Fulop, Masafumi Kimata, and Michael H. MacDougal, 16. SPIE, 2025. https://doi.org/10.1117/12.3056866.

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Mao, Yelu, Xiaoyu Shi, Ming-Sheng Shang, and Ying Zhang. "TCR." In the 2018 2nd International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3234804.3234819.

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Alrhmoun, S., M. S. Fisher, J. A. Lopatnikova, O. Y. Perik-Zavodskaia, M. O. Volynets, R. Y. Perik-Zavodskii, J. A. Shevchenko, et al. "ADVANCED CANCER IMMUNOTHERAPY: HARNESSING SINGLE-CELL SEQUENCING TO DISCOVER NATURALLY-OCCURRING ANTIGEN-SPECIFIC TCRS." In XI МЕЖДУНАРОДНАЯ КОНФЕРЕНЦИЯ МОЛОДЫХ УЧЕНЫХ: БИОИНФОРМАТИКОВ, БИОТЕХНОЛОГОВ, БИОФИЗИКОВ, ВИРУСОЛОГОВ, МОЛЕКУЛЯРНЫХ БИОЛОГОВ И СПЕЦИАЛИСТОВ ФУНДАМЕНТАЛЬНОЙ МЕДИЦИНЫ. IPC NSU, 2024. https://doi.org/10.25205/978-5-4437-1691-6-217.

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Adoptive cell therapy, particularly T cell receptor–engineered T (TCR-T) cell therapy, represents a cutting-edge and promising strategy for treating solid tumors [1]. Current methods for developing TCR-T cell therapies yield a limited number of candidate TCRs [2], missing the comprehensive view of the repertoire, which may impede the identification of the most effective TCRs. This limitation highlights the need for new techniques in TCR-T cell therapy development.
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Zhou, Jun, Zhenzhou Wu, Mengren Man, Yonghui Wu, Le Dinh Linh, Manna Dai, Yong Liu, and Rick Goh. "Llama-TCR: Generate De Novo TCR with Large Language Model." In 2024 IEEE Conference on Artificial Intelligence (CAI). IEEE, 2024. http://dx.doi.org/10.1109/cai59869.2024.00158.

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Tomimura, Toshio, Yasushi Koito, Taewan Do, Masaru Ishizuka, and Tomoyuki Hatakeyama. "On Simple Prediction Method for Thermal Contact Resistance Between Wavy Surfaces With Thermal Interface Material Under Low Mean Nominal Contact Pressure (Fundamental Study Based on 1-D Model)." In ASME 2015 International Technical Conference and Exhibition on Packaging and Integration of Electronic and Photonic Microsystems collocated with the ASME 2015 13th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/ipack2015-48302.

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The thermal contact resistance (TCR) is the crucial issue in the field of heat removal from systems like electronic equipment, satellite thermal control systems, and so on. To cope with the problem, a lot of studies have been done mainly for flat rough surfaces. However, as pointed out so far, there are still wide discrepancies among measured and predicted TCRs, even for similar materials. To investigate the key factors for the abovementioned discrepancies, a fundamental analysis was conducted in our previous study [1] using a simple contact surface model, which was composed of the unit cell model proposed by Tachibana [2] and Sanokawa [3]. Furthermore, by introducing a 2-D microscopic surface model, which consists of random numbers and Abbott’s bearing area curve, the effects of surface waviness and roughness on the temperature fields near the contact interface have been investigated microscopically [4]. In this study, based on a 1-D wavy surface model, a fundamental study has been conducted to predict TCR and the thermal contact conductance (TCC), which is a reciprocal of TCR, between wavy surfaces with the thermal interface material (TIM) under a relatively low mean nominal contact pressure of 0.1–1.0 MPa. From comparison between the calculated and measured results, it has been shown that, in spite of a simple 1-D analysis, the present model predicts the temperature drop at the contact interface, which is obtained as the product of TCR and the heat rate flowing through TIM, within some 10 to 60% error for a TIM with the thermal conductivity of 2.3 W/(m·K) and the initial thickness of 0.5, 1 and 2 mm.
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Wołczyn´ski, Waldemar S., Edward Guzik, Wojciech Wajda, and Bogusz Kania. "Columnar → Equiaxed Structure Transition in Solidifying Rolls." In 2010 14th International Heat Transfer Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/ihtc14-23048.

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As the first step of simulation, a temperature field for solidifying cast steel and cast iron roll was created. The convection in the liquid is not comprised since in the first approximation, the convection does not influence the analysed occurrence of the C → E (columnar to equiaxed grains) transition in the roll. The obtained temperature field allows to study the dynamics of its behavior observed in the middle of the mould thickness. This midpoint of the mould thickness was treated as an operating point for the C → E transition. A full accumulation of the heat in the mould was postulated for the C → E transition. Thus, a plateau at the T(t) curve was observed at the midpoint. The range of the plateau existence tC ↔ tE corresponded to the incubation period, tCR ↔ tER that appeared before fully equiaxed grains formation. At the second step of simulation, the thermal gradients field was studied. Three ranges were distinguished: a/ for the formation of the columnar structure (the C–zone): (T˙≫0and(G|t&amp;lt;tCR−G|t=tCR)≫0), b/ for the C → E transition (from columnar to fully equiaxed structure): (T˙≈0and(G|t=tCR−G|t=tER)≈0), c/ for the formation of the fully equiaxed structure (the E–zone): (T˙&amp;lt;0and(G|t=tER−G|t&amp;gt;tER)≈0). The columnar structure formation was significantly slowed down during incubation period. It resulted from a competition between columnar growth and equiaxed growth expected at that period of time. The (G|t=tCR − G|t=tER) ≈ 0) relationship was postulated to correspond well with the critical thermal gradient, Gcrit.. A simulation was performed for the cast steel and cast iron rolls solidifying as if in industrial condition. Since the incubation divides the roll into two zones (columnar and equiaxed) some experiments dealing with solidification were made on semi-industrial scale. A macrosegregation equation for both mentioned zones was formulated. It was based on a recent equation for redistribution after back-diffusion. The role of the back-diffusion parameter was emphasized as a factor responsible for the redistribution in columnar structure and equiaxed structure.
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Newby, Richard A., Wen-Ching Yang, and Ronald L. Bannister. "Use of Thermochemical Recuperation in Combustion Turbine Power Systems." In ASME 1997 International Gas Turbine and Aeroengine Congress and Exhibition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/97-gt-044.

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The performance and practicality of heavy duty combustion turbine power systems incorporating thermochemical recuperation (TCR) of natural gas has been estimated to assess the potential merits of this technology. Process models of TCR combustion turbine power systems based on the Westinghouse 501F combustion turbine were developed to conduct the performance evaluation. Two TCR schemes were assessed — Steam-TCR and Flue Gas-TCR. Compared to conventional combustion turbine power cycles, the TCR power cycles show the potential for significant plant heat rate improvements, but their practicality is an issue. Significant development remains to verify and commercialize TCR for combustion turbine power systems.
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Dretvik, Svein-Egil, Stian Svardal, and Steinar Kristoffersen. "Kristin Titanium Catenary Risers (TCR)." In ASME 2003 22nd International Conference on Offshore Mechanics and Arctic Engineering. ASMEDC, 2003. http://dx.doi.org/10.1115/omae2003-37352.

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The gas export from A˚sgard B has experienced vortex induced vibrations (VIV) internally in the flow caused by the irregularities in the carcass of the flexible risers. The VIV is amplified through resonance in the topside piping causing vibrations and fatigue resulting in gas leakage. So far extensive work have been carried out without succeeding in establishing predictable model for description of the VIV phenomena. For the Kristin project Titanium Catenary Risers (TCR) have been developed as an alternative to gas export through flexible risers. This paper will present the work performed to establish the TCR concept including design, production, installation and qualification.
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Reports on the topic "TCR"

1

Russell, Michael, Vincent Paquit, Luke Scime, and Alka Singh. TCR Data Management Plan. Office of Scientific and Technical Information (OSTI), March 2021. http://dx.doi.org/10.2172/1814318.

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2

Huning, Alex, and Randall Fair. TCR Postulated Accident and MHA Dose Assessment. Office of Scientific and Technical Information (OSTI), March 2021. http://dx.doi.org/10.2172/1778087.

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3

Shirvan, Koroush. Validation of Robustness in TCR Design Strategies. Office of Scientific and Technical Information (OSTI), March 2023. http://dx.doi.org/10.2172/1964002.

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4

Dehoff, Ryan, and Michael Russell. Quality Procedures for TCR Metal Core Structure Advanced Manufacturing Process. Office of Scientific and Technical Information (OSTI), September 2020. http://dx.doi.org/10.2172/1814370.

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5

Schappel, Danny, and Kurt Terrani. Key Material Properties for Thermo-Structural Analysis of TCR Core Components. Office of Scientific and Technical Information (OSTI), August 2019. http://dx.doi.org/10.2172/1558508.

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6

Scime, Luke, Michael Sprayberry, David Collins, Alka Singh, Chase Joslin, Ryan Duncan, Joseph Simpson, et al. Report on diagnostic and predictive capabilities of the TCR digital platform. Office of Scientific and Technical Information (OSTI), September 2021. http://dx.doi.org/10.2172/1831630.

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7

Li, Meimei, Xuan Zhang, Wei-Ying Chen, and Florent Heidet. Progress Report on the Assessment of the Material Performance for TCR Applications. Office of Scientific and Technical Information (OSTI), March 2020. http://dx.doi.org/10.2172/1608042.

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8

Li, Meimei, Xuan Zhang, Wei-Ying Chen, and Florent Heidet. Progress Report on the Assessment of the Material Performance for TCR Applications. Office of Scientific and Technical Information (OSTI), September 2020. http://dx.doi.org/10.2172/1701716.

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9

Field, Kevin, Joseph Simpson, Maxim Gussev, Hsin Wang, Meimei Li, Xuan Zhang, Xiang Chen, et al. Handbook of advanced manufactured material properties from TCR structure builds at ORNL – FY19. Office of Scientific and Technical Information (OSTI), September 2019. http://dx.doi.org/10.2172/1817605.

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10

Huning, Alex, Randall Fair, Alyson Coates, and Bruce Lin. TCR Input to NUREG-1537 Process for Advanced Nuclear Technologies Derived from Additive Manufacturing. Office of Scientific and Technical Information (OSTI), June 2021. http://dx.doi.org/10.2172/1805005.

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