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Journal articles on the topic 'T cell'

To see the other types of publications on this topic, follow the link: T cell.

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Ohshima, Kôichi, Junji Suzumiya, and Masahiro Kikuchi. "T cell rich B cell lymphoma." Journal of the Japan Society of the Reticuloendothelial System 36, no. 5-6 (1996): 391–93. http://dx.doi.org/10.3960/jslrt1961.36.391.

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2

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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3

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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4

CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.

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5

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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6

Hill, LaQuisa C., Rayne H. Rouce, and Maksim Mamonkin. "CAR T-Cells for T-cell Lymphoma." Clinical Lymphoma Myeloma and Leukemia 21 (September 2021): S173—S174. http://dx.doi.org/10.1016/s2152-2650(21)01255-6.

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7

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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8

Rimpo, Kenji, Yumiko Kagawa, and Tetsushi Yamagami. "T-cell-rich B-cell lymphoma in a dog." Journal of Japan Veterinary Cancer Society 4, no. 1 (2013): 1–5. http://dx.doi.org/10.12951/jvcs.2012-001.

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9

Zinkernagel, Rolf M., Demetrius Moskophidis, Thomas Kundig, Stephan Oehen, Hanspeter Pircher, and Hans Hengartner. "Effector T-Cell Induction and T-Cell Memory versus Peripheral Deletion of T Cells." Immunological Reviews 133, no. 1 (June 1993): 199–223. http://dx.doi.org/10.1111/j.1600-065x.1993.tb01517.x.

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10

Yano, Hiroki, Takashi Ishida, Atsushi Inagaki, Toshihiko Ishii, Shigeru Kusumoto, Hirokazu Komatsu, Shinsuke Iida, Atae Utsunomiya, and Ryuzo Ueda. "Regulatory T-cell function of adult T-cell leukemia/lymphoma cells." International Journal of Cancer 120, no. 9 (2007): 2052–57. http://dx.doi.org/10.1002/ijc.22536.

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11

Hong, Li, Tonya J. Webb, and David S. Wilkes. "Dendritic cell–T cell interactions: CD8αα expressed on dendritic cells regulates T cell proliferation." Immunology Letters 108, no. 2 (February 2007): 174–78. http://dx.doi.org/10.1016/j.imlet.2006.12.003.

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12

Toner, Keri, Catherine M. Bollard, and Hema Dave. "T-cell therapies for T-cell lymphoma." Cytotherapy 21, no. 9 (September 2019): 935–42. http://dx.doi.org/10.1016/j.jcyt.2019.04.058.

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13

Fitch, F. W. "T-cell clones and T-cell receptors." Microbiological Reviews 50, no. 1 (1986): 50–69. http://dx.doi.org/10.1128/mmbr.50.1.50-69.1986.

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14

Fitch, F. W. "T-cell clones and T-cell receptors." Microbiological Reviews 50, no. 1 (1986): 50–69. http://dx.doi.org/10.1128/mr.50.1.50-69.1986.

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15

Leisegang, Matthias, Adriana Turqueti-Neves, Boris Engels, Thomas Blankenstein, Dolores J. Schendel, Wolfgang Uckert, and Elfriede Noessner. "T-Cell Receptor Gene–Modified T Cells with Shared Renal Cell Carcinoma Specificity for Adoptive T-Cell Therapy." Clinical Cancer Research 16, no. 8 (April 14, 2010): 2333–43. http://dx.doi.org/10.1158/1078-0432.ccr-09-2897.

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16

Hogquist, Kristin A., Michael A. Weinreich, and Stephen C. Jameson. "T‐cell migration: Kruppeled T cells move again." Immunology & Cell Biology 86, no. 4 (April 2008): 297–98. http://dx.doi.org/10.1038/icb.2008.20.

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17

Notarangelo, Luigi D. "Functional T Cell Immunodeficiencies (with T Cells Present)." Annual Review of Immunology 31, no. 1 (March 21, 2013): 195–225. http://dx.doi.org/10.1146/annurev-immunol-032712-095927.

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18

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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19

Gérard, Audrey, Omar Khan, Peter Beemiller, Erin Oswald, Joyce Hu, Mehrdad Matloubian, and Matthew F. Krummel. "Secondary T cell–T cell synaptic interactions drive the differentiation of protective CD8+ T cells." Nature Immunology 14, no. 4 (March 10, 2013): 356–63. http://dx.doi.org/10.1038/ni.2547.

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20

Thümmler, Katja, Jan Leipe, Andreas Ramming, Hendrik Schulze-Koops, and Alla Skapenko. "Immune regulation by peripheral suppressor T cells induced upon homotypic T cell/T cell interactions." Journal of Leukocyte Biology 88, no. 5 (July 22, 2010): 1041–50. http://dx.doi.org/10.1189/jlb.0310122.

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21

Aandahl, Einar Martin, Knut Martin Torgersen, and Kjetil Taskén. "CD8+ regulatory T cells—A distinct T-cell lineage or a transient T-cell phenotype?" Human Immunology 69, no. 11 (November 2008): 696–99. http://dx.doi.org/10.1016/j.humimm.2008.08.291.

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22

Mohapatra, Manisha, and Yerraguntala Subramanya Sarma. "T-Cell/ Histiocyte-Rich Large B-Cell Lymphoma of Posterior Mediastinum." Annals of Pathology and Laboratory Medicine 6, no. 6 (June 24, 2019): C63–66. http://dx.doi.org/10.21276/apalm.2389.

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23

Chinnikatti, Shravana kumar, Soumya shravan, H. N. Asikur Rahaman, and Shraavya Shraavya. "New Treatments for Synovial Cell Sarcoma with Genetically Modified T-Cell?" Cancer Research and Cellular Therapeutics 6, no. 3 (May 16, 2022): 01–02. http://dx.doi.org/10.31579/2640-1053/113.

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Synovial cell sarcoma is rare but very aggressive tumour if not treated early, due to the painless nature of this tumour patients normally come in late and advances stage, can occur in bones, muscle cells, cartilages, ligaments and de-novo from pleuripotent stem cells from asnywhere in the body but most commonly arm, leg, or foot, and near joints such as the wrist or ankle and possibly from any joints in the body, even from soft tissues of lung and abdomen, the other name for this tumour is called malignant synovioma.The 5 year survival after the effective primary treatment is 30-75% and the survival rate is less than 5% if the tumour recurred within 1 year of primary treatment and that’s why new treatments are explored continuously. Due to late recognition and diagnosis of this rare tumour leads to many problems in treatment and in disease course. This tumour can occur at any age but is most common in growing periods like teen agers and adolescents. This tumour can spread to any organ in the body but most commonly distant metastases occur in lungs. Synovial sarcomas actually a misnomer as previously thought, now with advances in cell structure advances, These tumours can occur not only from synovial cells but from any cell of bone, muscle, tendon, ligaments and cartilage forming cells and supporting cells. These tumours occur with equal propensity in both men and women of younger age. If diagnosed early and treated early with surgery alone patients can be cured completely without any morbidity and mortality

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24

Udhayakumar, Venkatachalam, Bondada Subbarao, Aruna Seth, Mitzi Nagarkatti, and Prakash S. Nagarkatti. "Impaired autoreactive T cell-induced T cell-T cell interaction in aged mice." Cellular Immunology 116, no. 2 (October 1988): 299–307. http://dx.doi.org/10.1016/0008-8749(88)90232-8.

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25

Ramming, Andreas, Katja Thümmler, Hendrik Schulze-Koops, and Alla Skapenko. "Homotypic T-cell/T-cell interaction induces T-cell activation, proliferation, and differentiation." Human Immunology 70, no. 11 (November 2009): 873–81. http://dx.doi.org/10.1016/j.humimm.2009.08.003.

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26

Chen, Shuming, Naoto Ishii, Shouji Ine, Syuichi Ikeda, Taku Fujimura, Lishomwa C. Ndhlovu, Pejman Soroosh, et al. "Regulatory T cell-like activity of Foxp3+ adult T cell leukemia cells." International Immunology 18, no. 2 (December 16, 2005): 269–77. http://dx.doi.org/10.1093/intimm/dxh366.

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27

Jamal, Iffat. "Hepatosplenic T Cell Lymphoma: A Rare Disease." Cytology & Histology International Journal 4, no. 1 (2020): 1–3. http://dx.doi.org/10.23880/chij-16000118.

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Hepatosplenic T cell lymphoma (HSTCL) is an uncommon neoplasm comprising 5% of peripheral T-cell lymphomas. We report an uncommon case of Peripheral T-cell lymphoma that is characterized by primary extranodal disease with malignant T cell proliferation in spleen, liver and bone marrow. 19 year old male patient presented with fever, weakness and pain abdomen for 2 months. On clinical examination he was pale and had massive hepatosplenomegaly. The diagnosis was quite challenging as thorough clinical, hematological and immunophenotypic correlation was required.

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28

KA, Awadhesh. "Basics of T Cell Development and Activation." Journal of Embryology & Stem Cell Research 2, no. 1 (2018): 1–4. http://dx.doi.org/10.23880/jes-16000103.

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29

Russi, Abigail E., Margaret E. Walker-Caulfield, Yong Guo, Claudia F. Lucchinetti, and Melissa A. Brown. "Meningeal mast cell-T cell crosstalk regulates T cell encephalitogenicity." Journal of Autoimmunity 73 (September 2016): 100–110. http://dx.doi.org/10.1016/j.jaut.2016.06.015.

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30

Gonthier, Marie, Régine Llobera, Jacques Arnaud, and Bent Rubin. "Self-Reactive T Cell Receptor-Reactive CD8+ T Cells Inhibit T Cell Lymphoma Growth In Vivo." Journal of Immunology 173, no. 11 (November 19, 2004): 7062–69. http://dx.doi.org/10.4049/jimmunol.173.11.7062.

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31

Jiang, H., H. Kashleva, L. X. Xu, J. Forman, L. Flaherty, B. Pernis, N. S. Braunstein, and L. Chess. "T cell vaccination induces T cell receptor V -specific Qa-1-restricted regulatory CD8+ T cells." Proceedings of the National Academy of Sciences 95, no. 8 (April 14, 1998): 4533–37. http://dx.doi.org/10.1073/pnas.95.8.4533.

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32

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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33

Vanham, Guido, Lieve Penne, Heidi Allemeersch, Luc Kestens, Betty Willems, Guido van der Groen, Kuan-Teh Jeang, Zahra Toossi, and Elizabeth Rich. "Modeling HIV transfer between dendritic cells and T cells: importance of HIV phenotype, dendritic cell– T cell contact and T-cell activation." AIDS 14, no. 15 (October 2000): 2299–311. http://dx.doi.org/10.1097/00002030-200010200-00011.

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34

Khanolkar, Aaruni, Michael J. Fuller, and Allan J. Zajac. "CD4 T Cell-Dependent CD8 T Cell Maturation." Journal of Immunology 172, no. 5 (February 20, 2004): 2834–44. http://dx.doi.org/10.4049/jimmunol.172.5.2834.

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35

Boismenu, Richard, and Wendy L. Havran. "T-Cell Development: T-cell lineage commitment revisited." Current Biology 5, no. 8 (August 1995): 829–31. http://dx.doi.org/10.1016/s0960-9822(95)00164-3.

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36

Lindsey, JW, RH Kerman, and JS Wolinsky. "T cell-T cell activation in multiple sclerosis." Multiple Sclerosis Journal 3, no. 4 (August 1997): 238–42. http://dx.doi.org/10.1177/135245859700300404.

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Activated T cells are able to stimulate proliferation in resting T cells through an antigen non-specific mechanism. The in vivo usefulness of this T cell-T cell activation is unclear, but it may serve to amplify immune responses. T cell-T cell activation could be involved in the well-documented occurrence of multiple sclerosis (MS) exacerbations following viral infections. Excessive activation via this pathway could also be a factor in the etiology of MS. We tested the hypothesis that excessive T cell-T cell activation occurs in MS patients using in vitro proliferation assays comparing T cells from MS patients to T cells from controls. When tested as responder cells, T cells from MS patients proliferated slightly less after stimulation with previously activated cells than T cells from controls. When tested as stimulator cells, activated cells from MS patients stimulated slightly more non-specific proliferation than activated cells from controls. Neither of these differences were statistically significant We conclude that T cell proliferation in response to activated T cells is similar in MS and controls.

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37

Lechler, Robert, Jian-Guo Chai, Federica Marelli-Berg, and Giovanna Lombardi. "T–cell anergy and peripheral T–cell tolerance." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1409 (May 29, 2001): 625–37. http://dx.doi.org/10.1098/rstb.2001.0844.

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The discovery that T–cell recognition of antigen can have distinct outcomes has advanced understanding of peripheral T–cell tolerance, and opened up new possibilities in immunotherapy. Anergy is one such outcome, and results from partial T–cell activation. This can arise either due to subtle alteration of the antigen, leading to a lower–affinity cognate interaction, or due to a lack of adequate co–stimulation. The signalling defects in anergic T cells are partially defined, and suggest that T–cell receptor (TCR) proximal, as well as downstream defects negatively regulate the anergic T cell's ability to be activated. Most importantly, the use of TCR–transgenic mice has provided compelling evidence that anergy is an in vivo phenomenon, and not merely an in vitro artefact. These findings raise the question as to whether anergic T cells have any biological function. Studies in rodents and in man suggest that anergic T cells acquire regulatory properties; the regulatory effects of anergic T cells require cell to cell contact, and appear to be mediated by inhibition of antigen–presenting cell immunogenicity. Close similarities exist between anergic T cells, and the recently defined CD4 + CD25 + population of spontaneously arising regulatory cells that serve to inhibit autoimmunity in mice. Taken together, these findings suggest that a spectrum of regulatory T cells exists. At one end of the spectrum are cells, such as anergic and CD4 + CD25 + T cells, which regulate via cell–to–cell contact. At the other end of the spectrum are cells which secrete antiinflammatory cytokines such as interleukin 10 and transforming growth factor–β. The challenge is to devise strategies that reliably induce T–cell anergy in vivo , as a means of inhibiting immunity to allo– and autoantigens.

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38

Gill, Ronald G. "T-cell-T-cell collaboration in allograft responses." Current Opinion in Immunology 5, no. 5 (October 1993): 782–87. http://dx.doi.org/10.1016/0952-7915(93)90137-h.

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39

Testa, Ugo, Patrizia Chiusolo, Elvira Pelosi, Germana Castelli, and Giuseppe Leone. "CAR-T CELL THERAPY FOR T-CELL MALIGNANCIES." Mediterranean Journal of Hematology and Infectious Diseases 16, no. 1 (February 29, 2024): e2024031. http://dx.doi.org/10.4084/mjhid.2024.031.

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Chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of B-cell lymphoid neoplasia and, in some instances, improved disease outcomes. Thus, six FDA-approved commercial CAR-T cell products that target antigens preferentially expressed on malignant B-cells or plasma cells have been introduced in the therapy of B-cell lymphomas, B-ALLs and multiple myeloma. These therapeutic successes have triggered the application of CAR-T cell therapy to other hematologic tumors, including T-cell malignancies. However, the success of CAR-T cell therapies in T-cell neoplasms was considerably more limited to the existence of some limiting factors, such as the sharing of mutual antigens between normal T-cells and CAR-T cells, and malignant cells, determining fratricide events and severe T-cell aplasia; contamination of CAR-T cells used for CAR transduction with contaminating malignant T-cells. Allogeneic CAR-T products can avoid tumor contamination but raise other problems related to immunological incompatibility. In spite of these limitations, there has been significant progress in CD7- and CD5-targeted CAR-T cell therapy of T-cell malignancies in the last few years.

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40

Mitchell, Emily, and George S. Vassiliou. "T-Cell Cancer after CAR T-Cell Therapy." New England Journal of Medicine 390, no. 22 (June 13, 2024): 2120–21. http://dx.doi.org/10.1056/nejme2405538.

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41

Yu, Guang, Hongyu Luo, Yulian Wu, and Jiangping Wu. "EphrinB1 Is Essential in T-cell-T-cell Co-operation during T-cell Activation." Journal of Biological Chemistry 279, no. 53 (October 22, 2004): 55531–39. http://dx.doi.org/10.1074/jbc.m410814200.

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42

Jameson, Stephen C. "T cell homeostasis: Keeping useful T cells alive and live T cells useful." Seminars in Immunology 17, no. 3 (June 2005): 231–37. http://dx.doi.org/10.1016/j.smim.2005.02.003.

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43

Reinhardt, Julia, Virag Sharma, Antigoni Stavridou, Annett Lindner, Susanne Reinhardt, Andreas Petzold, Mathias Lesche, Fabian Rost, Ezio Bonifacio, and Anne Eugster. "Distinguishing activated T regulatory cell and T conventional cells by single‐cell technologies." Immunology 166, no. 1 (March 2, 2022): 121–37. http://dx.doi.org/10.1111/imm.13460.

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44

Dubois, Sigrid, Lionel Feigenbaum, Thomas A. Waldmann, and Jürgen R. Müller. "NK cells prevent T cell lymphoma development in T cell receptor-transgenic mice." Cellular Immunology 352 (June 2020): 104081. http://dx.doi.org/10.1016/j.cellimm.2020.104081.

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45

Smith, Christopher M., Nicholas S. Wilson, Jason Waithman, Jose A. Villadangos, Francis R. Carbone, William R. Heath, and Gabrielle T. Belz. "Cognate CD4+ T cell licensing of dendritic cells in CD8+ T cell immunity." Nature Immunology 5, no. 11 (October 10, 2004): 1143–48. http://dx.doi.org/10.1038/ni1129.

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46

Taams, Leonie S., Annemiek J. M. L. van Rensen, Martien C. M. Poelen, Cécile A. C. M. van Els, Arit C. Besseling, Josée P. A. Wagenaar, Willem van Eden, and Marca H. M. Wauben. "Anergic T cells actively suppress T cell responses via the antigen-presenting cell." European Journal of Immunology 28, no. 9 (September 1998): 2902–12. http://dx.doi.org/10.1002/(sici)1521-4141(199809)28:09<2902::aid-immu2902>3.0.co;2-b.

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47

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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48

Johnson, P. Connor, and Jeremy S. Abramson. "Engineered T Cells: CAR T Cell Therapy and Beyond." Current Oncology Reports 24, no. 1 (January 2022): 23–31. http://dx.doi.org/10.1007/s11912-021-01161-4.

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49

Chapman, Paul B. "Programming T cells for adoptive T cell transfer therapy." Pigment Cell & Melanoma Research 23, no. 2 (February 1, 2010): 155–56. http://dx.doi.org/10.1111/j.1755-148x.2010.00681.x.

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50

Fahlén, Linda, Linda Öberg, Thomas Brännström, Nelson K. S. Khoo, Urban Lendahl, and Charles L. Sentman. "Ly49A expression on T cells alters T cell selection." International Immunology 12, no. 2 (February 2000): 215–22. http://dx.doi.org/10.1093/intimm/12.2.215.

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