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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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Abstract (sommario):
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

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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4

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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5

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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6

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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7

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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8

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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9

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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Abstract (sommario):
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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10

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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11

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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12

Kotulová, Jana, (Kufova) Zuzana Chyra, Zhongfei Tao, Piotr Celichowski, Jana Mihalyova, Sandra Charvátová, and Roman Hajek. "Impact of T cell characteristics on CAR-T cell therapy in hematological malignancies." Blood Cancer Journal 14, no. 1 (December 3, 2024): 1–10. https://doi.org/10.1038/s41408-024-01193-6.

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13

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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14

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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Abstract (sommario):
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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15

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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16

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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17

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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18

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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Abstract (sommario):
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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19

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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Abstract (sommario):
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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20

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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21

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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Abstract (sommario):
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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22

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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23

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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24

Matsumoto, Yosuke, Hisao Nagoshi, Mihoko Yoshida, Seiichi Kato, Junya Kuroda, Kazuho Shimura, Hiroto Kaneko, Shigeo Horiike, Shigeo Nakamura, and Masafumi Taniwaki. "Expression of Master Regulators of T-cell, Helper T-cell and Follicular Helper T-cell Differentiation in Angioimmunoblastic T-cell Lymphoma." Internal Medicine 56, no. 21 (2017): 2851–56. http://dx.doi.org/10.2169/internalmedicine.8570-16.

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25

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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26

Manolios, Nicholas, Simon Collier, Jude Taylor, John Pollard, Leonard C. Harrison, and Veronica Bender. "T-cell antigen receptor transmembrane peptides modulate T-cell function and T cell-mediated disease." Nature Medicine 3, no. 1 (January 1997): 84–88. http://dx.doi.org/10.1038/nm0197-84.

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27

Salzmann, Michael, and Martin F. Bachmann. "The role of T cell receptor dimerization for T cell antagonism and T cell specificity." Molecular Immunology 35, no. 5 (April 1998): 271–77. http://dx.doi.org/10.1016/s0161-5890(98)00035-2.

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28

Hashimoto, Y., and K. J. Blank. "T cell receptor genes and T cell development in virus-transformed early T cell lines." Journal of Immunology 144, no. 4 (February 15, 1990): 1518–25. http://dx.doi.org/10.4049/jimmunol.144.4.1518.

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Abstract (sommario):
Abstract We have derived T cell lines from mice inoculated with Gross leukemia virus, which appear to represent early T cell developmental stages and to reflect normal T cell development. These cell lines may provide a breakthrough in the study of T cell development as Abelson transformants have done for the study of B cell development. Analysis of the TCR gene expression in these cell lines reveals that the sequence of rearrangement and expression of each TCR gene is not strictly ordered. Expression of RNA for the TCR alpha and -beta genes appears to be coordinated with rearrangement at the alpha and beta loci. This is not the case for gamma gene expression. Availability of the homogeneous populations of cells represented in these cells lines allows for a more detailed molecular analysis of T cell development than was previously possible.
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29

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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30

Bruneau, Julie, Danielle Canioni, Amédée Renand, Teresa Marafioti, Jennifer C. Paterson, Nadine Martin-Garcia, Philippe Gaulard, et al. "Regulatory T-Cell Depletion in Angioimmunoblastic T-Cell Lymphoma." American Journal of Pathology 177, no. 2 (August 2010): 570–74. http://dx.doi.org/10.2353/ajpath.2010.100150.

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31

Rodríguez-Pinilla, Socorro María, Lidia Atienza, Cristina Murillo, Alberto Pérez-Rodríguez, Santiago Montes-Moreno, Giovanna Roncador, Carlos Pérez-Seoane, Purificación Domínguez, Francisca I. Camacho, and Miguel A. Piris. "Peripheral T-cell Lymphoma With Follicular T-cell Markers." American Journal of Surgical Pathology 32, no. 12 (December 2008): 1787–99. http://dx.doi.org/10.1097/pas.0b013e31817f123e.

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32

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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33

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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34

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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35

DiPersio, John F., Karl Staser, and Matthew Cooper. "Immunotherapy for T-Cell ALL and T-Cell NHL." Clinical Lymphoma Myeloma and Leukemia 20 (September 2020): S56—S58. http://dx.doi.org/10.1016/s2152-2650(20)30462-6.

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36

Moltedo, Bruno, Saskia Hemmers, and Alexander Y. Rudensky. "Regulatory T Cell Ablation Causes Acute T Cell Lymphopenia." PLoS ONE 9, no. 1 (January 23, 2014): e86762. http://dx.doi.org/10.1371/journal.pone.0086762.

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37

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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38

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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39

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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40

Mackall, Crystal L., Frances T. Hakim, and Ronald E. Gress. "Restoration of T-cell homeostasis after T-cell depletion." Seminars in Immunology 9, no. 6 (December 1997): 339–46. http://dx.doi.org/10.1006/smim.1997.0091.

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41

Bajaj, Anubha. "Ripened and Revamped-Adult T Cell Leukaemia/ Lymphoma." Clinical Pathology & Research Journal 7, no. 1 (2023): 1–6. http://dx.doi.org/10.23880/cprj-16000151.

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Abstract (sommario):
Adult T cell leukaemia/ lymphoma is an aggressive T cell malignant disorder comprised of significantly pleomorphic, miniature to intermediate, mature CD4+ T cells. Factors such as demographic distribution within HTLV1 endemic zones, hypercalcemia, cutaneous lesions and a leukemic phase contribute to disease emergence. Adult T cell leukaemia/ lymphoma incriminates peripheral blood, lymph nodes, spleen, cutaneous surfaces, pulmonary or hepatic parenchyma, gastrointestinal tract and central nervous system. Bone marrow may demonstrate diffuse, interstitial or sinusoidal pattern of neoplastic occurrence. Generally, tumour cells are permeated with basophilic cytoplasm, absent intracytoplasmic granules, irregular or poly-lobulated nuclei with homogeneous, condensed nuclear chromatin and miniature nucleoli.
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42

Soroosh, Pejman, Shouji Ine, Kazuo Sugamura, and Naoto Ishii. "OX40-OX40 Ligand Interaction through T Cell-T Cell Contact Contributes to CD4 T Cell Longevity." Journal of Immunology 176, no. 10 (May 2, 2006): 5975–87. http://dx.doi.org/10.4049/jimmunol.176.10.5975.

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43

Penaloza-MacMaster, Pablo, David Masopust, and Rafi Ahmed. "T-cell reconstitution without T-cell immunopathology in two models of T-cell-mediated tissue destruction." Immunology 128, no. 2 (October 2009): 164–71. http://dx.doi.org/10.1111/j.1365-2567.2009.03080.x.

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44

Wucherpfennig, K. W., P. Hollsberg, J. H. Richardson, D. Benjamin, and D. A. Hafler. "T-cell activation by autologous human T-cell leukemia virus type I-infected T-cell clones." Proceedings of the National Academy of Sciences 89, no. 6 (March 15, 1992): 2110–14. http://dx.doi.org/10.1073/pnas.89.6.2110.

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45

Ge, Q., D. Palliser, H. N. Eisen, and J. Chen. "Homeostatic T cell proliferation in a T cell-dendritic cell coculture system." Proceedings of the National Academy of Sciences 99, no. 5 (February 19, 2002): 2983–88. http://dx.doi.org/10.1073/pnas.052714199.

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46

Ehrenstein, M. R., and B. Hahn. "T cell—B cell interactions." Lupus 11, no. 12 (December 2002): 790–92. http://dx.doi.org/10.1191/0961203302lu319oa.

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47

Mekori, Yoseph A., and Dean D. Metcalfe. "Mast cell–T cell interactions." Journal of Allergy and Clinical Immunology 104, no. 3 (September 1999): 517–23. http://dx.doi.org/10.1016/s0091-6749(99)70316-7.

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48

Jutila, Mark A. "T cell/endothelial cell interactions." Veterinary Immunology and Immunopathology 54, no. 1-4 (November 1996): 105–10. http://dx.doi.org/10.1016/s0165-2427(96)05691-7.

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49

Sprent, Jonathan. "T cell–B cell collaboration." Nature Reviews Immunology 17, no. 9 (May 30, 2017): 532. http://dx.doi.org/10.1038/nri.2017.62.

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50

Mitchison, N. A. "T-cell–B-cell cooperation." Nature Reviews Immunology 4, no. 4 (April 2004): 308–12. http://dx.doi.org/10.1038/nri1334.

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