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Journal articles on the topic 'Human t-cell leukemia viru'

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Published: 11 March 2023

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1

Norris, Philip J., Dale F. Hirschkorn, Deborah A. DeVita, Tzong-Hae Lee, and Edward L. Murphy. "Human T cell leukemia virus type 1 infection drives spontaneous proliferation of natural killer cells." Virulence 1, no. 1 (January 2010): 19–28. http://dx.doi.org/10.4161/viru.1.1.9868.

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2

Sohn, CC, DW Blayney, JL Misset, G. Mathe, G. Flandrin, EM Moran, FC Jensen, CD Winberg, and H. Rappaport. "Leukopenic chronic T cell leukemia mimicking hairy cell leukemia: association with human retroviruses." Blood 67, no. 4 (April 1, 1986): 949–56. http://dx.doi.org/10.1182/blood.v67.4.949.949.

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Abstract We report two cases of a T cell lymphoproliferative disease not previously described, with cytologic and clinical features similar to those associated with Galton's “prolymphocytic” leukemia (PL). Our patients, like those with Galton's PL, had massive splenomegaly and minimal or absent hepatomegaly and lymphadenopathy. In contrast, however, our patients had leukopenia, as well as low percentages of leukemic cells in the peripheral blood and in the bone marrow. In splenic imprints, the nuclear chromatin pattern of most of the leukemic cells was intermediate between those of mature lymphocytes and those of lymphoblasts, and the nuclei contained single, centrally located, conspicuous nucleoli. In sections of the spleen, the leukemic cells diffusely infiltrated the red pulp in a pattern strikingly similar to that of hairy cell leukemia; however, when the leukemic cells were studied cytochemically, the cytoplasmic acid phosphatase positivity was punctate and tartrate-sensitive. The leukemic cells were sheep erythrocyte rosette-positive and expressed T cell-associated antigens. Initially, both patients responded well to therapeutic splenectomy. One patient received combination chemotherapy after splenectomy and is alive and well 24 months after diagnosis. The other patient was in complete clinical remission for one year after splenectomy and received chemotherapy at relapse. He died, however, 23 months after splenectomy, with disseminated disease. IgG antibody titers against human T lymphotropic virus type I (HTLV-I) were detected in one patient and against HTLV-II in the other. The leukemia in these patients represents a distinct clinicopathologic entity within the spectrum of peripheral T cell lymphoproliferative diseases that includes Galton's PL of T cell derivation, T cell chronic lymphocytic leukemia, T cell hairy cell leukemia, and adult T cell leukemia/lymphoma.

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3

Sohn, CC, DW Blayney, JL Misset, G. Mathe, G. Flandrin, EM Moran, FC Jensen, CD Winberg, and H. Rappaport. "Leukopenic chronic T cell leukemia mimicking hairy cell leukemia: association with human retroviruses." Blood 67, no. 4 (April 1, 1986): 949–56. http://dx.doi.org/10.1182/blood.v67.4.949.bloodjournal674949.

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We report two cases of a T cell lymphoproliferative disease not previously described, with cytologic and clinical features similar to those associated with Galton's “prolymphocytic” leukemia (PL). Our patients, like those with Galton's PL, had massive splenomegaly and minimal or absent hepatomegaly and lymphadenopathy. In contrast, however, our patients had leukopenia, as well as low percentages of leukemic cells in the peripheral blood and in the bone marrow. In splenic imprints, the nuclear chromatin pattern of most of the leukemic cells was intermediate between those of mature lymphocytes and those of lymphoblasts, and the nuclei contained single, centrally located, conspicuous nucleoli. In sections of the spleen, the leukemic cells diffusely infiltrated the red pulp in a pattern strikingly similar to that of hairy cell leukemia; however, when the leukemic cells were studied cytochemically, the cytoplasmic acid phosphatase positivity was punctate and tartrate-sensitive. The leukemic cells were sheep erythrocyte rosette-positive and expressed T cell-associated antigens. Initially, both patients responded well to therapeutic splenectomy. One patient received combination chemotherapy after splenectomy and is alive and well 24 months after diagnosis. The other patient was in complete clinical remission for one year after splenectomy and received chemotherapy at relapse. He died, however, 23 months after splenectomy, with disseminated disease. IgG antibody titers against human T lymphotropic virus type I (HTLV-I) were detected in one patient and against HTLV-II in the other. The leukemia in these patients represents a distinct clinicopathologic entity within the spectrum of peripheral T cell lymphoproliferative diseases that includes Galton's PL of T cell derivation, T cell chronic lymphocytic leukemia, T cell hairy cell leukemia, and adult T cell leukemia/lymphoma.

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4

Matsuoka, Masao. "Human T-cell leukemia virus type I and adult T-cell leukemia." Oncogene 22, no. 33 (August 2003): 5131–40. http://dx.doi.org/10.1038/sj.onc.1206551.

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5

Hori, T., T. Uchiyama, M. Tsudo, H. Umadome, H. Ohno, S. Fukuhara, K. Kita, and H. Uchino. "Establishment of an interleukin 2-dependent human T cell line from a patient with T cell chronic lymphocytic leukemia who is not infected with human T cell leukemia/lymphoma virus." Blood 70, no. 4 (October 1, 1987): 1069–72. http://dx.doi.org/10.1182/blood.v70.4.1069.1069.

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Abstract We established an interleukin 2 (IL-2)-dependent human T cell line, Kit 225, from a patient with T cell chronic lymphocytic leukemia (T-CLL) with OKT3+, -T4+, -T8- phenotype. Southern blot analysis showed that Kit 225 is not infected with human T cell leukemia/lymphoma virus (HTLV) type I or II, and is probably derived from the major clone in the fresh leukemic cells. Kit 225 cells express a large amount of IL 2 receptors constitutively and their growth is absolutely dependent on IL 2. No other stimuli, such as lectins or antigens, are required for maintaining the responsiveness to IL 2. As abnormal IL 2 receptor expression was also seen originally in the fresh leukemic cells, the establishment of this cell line with IL 2 suggests that IL 2-mediated T cell proliferation is involved in the leukemogenesis of some cases of HTLV-negative T-CLL.

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6

Hori, T., T. Uchiyama, M. Tsudo, H. Umadome, H. Ohno, S. Fukuhara, K. Kita, and H. Uchino. "Establishment of an interleukin 2-dependent human T cell line from a patient with T cell chronic lymphocytic leukemia who is not infected with human T cell leukemia/lymphoma virus." Blood 70, no. 4 (October 1, 1987): 1069–72. http://dx.doi.org/10.1182/blood.v70.4.1069.bloodjournal7041069.

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We established an interleukin 2 (IL-2)-dependent human T cell line, Kit 225, from a patient with T cell chronic lymphocytic leukemia (T-CLL) with OKT3+, -T4+, -T8- phenotype. Southern blot analysis showed that Kit 225 is not infected with human T cell leukemia/lymphoma virus (HTLV) type I or II, and is probably derived from the major clone in the fresh leukemic cells. Kit 225 cells express a large amount of IL 2 receptors constitutively and their growth is absolutely dependent on IL 2. No other stimuli, such as lectins or antigens, are required for maintaining the responsiveness to IL 2. As abnormal IL 2 receptor expression was also seen originally in the fresh leukemic cells, the establishment of this cell line with IL 2 suggests that IL 2-mediated T cell proliferation is involved in the leukemogenesis of some cases of HTLV-negative T-CLL.

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7

Valtieri, M., D. Santoli, D. Caracciolo, B. L. Kreider, S. W. Altmann, D. J. Tweardy, I. Gemperlein, F. Mavilio, B. Lange, and G. Rovera. "Establishment and characterization of an undifferentiated human T leukemia cell line which requires granulocyte-macrophage colony stimulatory factor for growth." Journal of Immunology 138, no. 11 (June 1, 1987): 4042–50. http://dx.doi.org/10.4049/jimmunol.138.11.4042.

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Abstract A human leukemia cell line (TALL-101) was established from the bone marrow of a patient with an undifferentiated acute T cell leukemia using the conditioned medium (CM) of the human T cell leukemia virus (HTLV) II-transformed human cell line J-LB1. Immunofluorescence analysis on the original leukemic cells indicated the presence of T cell markers (Leu-1, Tdt, and T11); however, the established TALL-101 cell line expressed only antigens commonly present on progenitor cells, thymocytes, and myelomonocytic cells, but not on mature T cells. A high percentage of TALL-101 cells displayed the Tac antigen which was down-regulated upon incubation in the presence of recombinant human (rH) interleukin 2 (IL 2). Interferon (IFN)-gamma induced the appearance of class II histocompatibility leukocyte antigens (HLA) and of a T cell marker (3A1), and enhanced the expression of transferrin receptors on these cells. Further evidence for a T cell lineage of the TALL-101 cell line was provided by both chromosomic and genotypic analysis showing a translocation in chromosome 14 typical of T cell leukemias, and a rearrangement of the T-beta receptor locus. The growth-promoting activity in the J-LB1-CM was identified as granulocyte-macrophage colony stimulatory factor (GM-CSF), a growth factor which stimulates proliferation of normal myelomonocytic cells and other progenitor cells, but not known to have an effect on T cells. Dose response curves of [3H]thymidine incorporation and growth indicated that TALL-101 cells were sensitive to very low concentrations of rHGM-CSF, 5 ng/ml inducing maximal proliferation in chemically defined medium. The TALL-101 cell line is strictly GM-CSF-dependent for growth: upon depletion of GM-CSF from the culture medium, the cells stop proliferating immediately and die within 1 to 2 wk. The overall data, showing that GM-CSF is able to support the growth of a highly undifferentiated T cell leukemia, strongly suggests that this factor might have similar growth promoting effects on other immature T cell leukemias, and possibly, on normal T cell progenitors.

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8

Nitta, Takayuki, Masayuki Kanai, Eiji Sugihara, Masakazu Tanaka, Binlian Sun, Toshiro Nagasawa, Shunro Sonoda, Hideyuki Saya, and Masanao Miwa. "Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells." Cancer Science 97, no. 9 (September 2006): 836–41. http://dx.doi.org/10.1111/j.1349-7006.2006.00254.x.

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9

Oliveira, Pedro Dantas, Lourdes Farre, and Achiléa Lisboa Bittencourt. "Adult T-cell leukemia/lymphoma." Revista da Associação Médica Brasileira 62, no. 7 (October 2016): 691–700. http://dx.doi.org/10.1590/1806-9282.62.07.691.

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Summary Adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature CD4+ T-cells caused by human T-cell lymphotropic virus type 1 (HTLV-1). Twenty million people are believed to be infected throughout the world, mostly in Japan, Africa, the Caribbean, and South America, particularly in Brazil and Peru. ATL affects about 5% of infected individuals and is classified in the following clinical forms: acute, lymphoma, primary cutaneous tumoral, chronic (favorable and unfavorable), and smoldering (leukemic and non-leukemic). Although it is considered an aggressive disease, there are cases with a long progression. We emphasize the importance of clinical classification as an indispensable element for evaluating prognosis and appropriate therapeutic approach. Since several cases have been published in Brazil and this disease is still poorly known, we decided to make a review paper for dissemination of clinical, hematological and pathological aspects, diagnosis, and therapy. The best way to reduce the occurrence of ATL would be halting the transmission of the virus through breastfeeding.

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10

Mori, Naoki, Youichi Nunokawa, Yasuaki Yamada, Shuichi Ikeda, Masao Tomonaga, and Naoki Yamamoto. "Expression of Human Inducible Nitric Oxide Synthase Gene in T-Cell Lines Infected With Human T-Cell Leukemia Virus Type-I and Primary Adult T-Cell Leukemia Cells." Blood 94, no. 8 (October 15, 1999): 2862–70. http://dx.doi.org/10.1182/blood.v94.8.2862.420k24_2862_2870.

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We examined the expression of messenger RNA (mRNA) of the human inducible nitric oxide synthase (hiNOS) gene in a panel of human T-cell lines. Reverse transcriptase-polymerase chain reaction showed that human T-cell leukemia virus type-I (HTLV-I)–infected T-cell lines (MT-1, SLB-1, and C5/MJ) expressed mRNA for the hiNOS, but TL-Om1 or uninfected Jurkat, H9, and CCRF-CEM did not. The MT-1, SLB-1, and C5/MJ cell lines are infected with HTLV-I and express the viral transactivator Tax, whereas TL-Om1 cells, although derived from adult T-cell leukemia (ATL) leukemic cells, do not express Tax. There was, thus, a correlation between Tax and hiNOS mRNA expression. The transcriptional regulatory region of the hiNOS gene was activated by Tax in Jurkat, in which endogenous hiNOS is induced by Tax. Deletion analysis showed that the region of hiNOS encompassing nucleotides −159 to −111 contained the minimum Tax-responsive elements. Mutations in the NF-κB element at position −115 and −106 bp in the hiNOS promoter were still activated by Tax, and a Tax mutant defective for activation of the NF-κB pathway retained the ability to activate the hiNOS promoter. In addition, overexpression of the dominant-negative mutants of IκB and I κBβ failed to reduce Tax-induced activation of hiNOS gene. Furthermore, hiNOS mRNA was detected in leukemic cells from ATL patients. Our results show that the hiNOS promoter contains a minimum Tax-responsive element located between nucleotides −159 and −111, and imply that the expression of the hiNOS gene is involved in the pathogenesis of HTLV-I–associated diseases.

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11

Panfil, Amanda R., Michael P. Martinez, Lee Ratner, and Patrick L. Green. "Human T-cell leukemia virus-associated malignancy." Current Opinion in Virology 20 (October 2016): 40–46. http://dx.doi.org/10.1016/j.coviro.2016.08.009.

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12

Ratner, Lee, William Harrington, Xuan Feng, Christian Grant, Steve Jacobson, Ariela Noy, Joseph Sparano, et al. "Human T Cell Leukemia Virus Reactivation with Progression of Adult T-Cell Leukemia-Lymphoma." PLoS ONE 4, no. 2 (February 10, 2009): e4420. http://dx.doi.org/10.1371/journal.pone.0004420.

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13

Greenberg, SJ, ES Jaffe, GD Ehrlich, NJ Korman, BJ Poiesz, and TA Waldmann. "Kaposi‧s sarcoma in human T-cell leukemia virus type I-associated adult T-cell leukemia." Blood 76, no. 5 (September 1, 1990): 971–76. http://dx.doi.org/10.1182/blood.v76.5.971.971.

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Abstract Kaposi's sarcoma (KS) developed in a patient with human T-cell leukemia virus type I (HTLV-I)-associated adult T-cell leukemia who was treated with a short-term course of monoclonal antibody immunotherapy. The presentation was transient and temporally related to the underlying clinical course. The association of KS in an HTLV-I infected, but not human immunodeficiency virus (HIV)-infected, individual should alert investigators to the occurrence of KS in retroviral-associated diseases other than acquired immunodeficiency disease syndrome. Recognition of the similarities and differences between HTLV-I and HIV infections may provide insights concerning the angiopathogenesis of KS.

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14

Greenberg, SJ, ES Jaffe, GD Ehrlich, NJ Korman, BJ Poiesz, and TA Waldmann. "Kaposi‧s sarcoma in human T-cell leukemia virus type I-associated adult T-cell leukemia." Blood 76, no. 5 (September 1, 1990): 971–76. http://dx.doi.org/10.1182/blood.v76.5.971.bloodjournal765971.

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Kaposi's sarcoma (KS) developed in a patient with human T-cell leukemia virus type I (HTLV-I)-associated adult T-cell leukemia who was treated with a short-term course of monoclonal antibody immunotherapy. The presentation was transient and temporally related to the underlying clinical course. The association of KS in an HTLV-I infected, but not human immunodeficiency virus (HIV)-infected, individual should alert investigators to the occurrence of KS in retroviral-associated diseases other than acquired immunodeficiency disease syndrome. Recognition of the similarities and differences between HTLV-I and HIV infections may provide insights concerning the angiopathogenesis of KS.

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15

Maeda, M., A. Shimizu, K. Ikuta, H. Okamoto, M. Kashihara, T. Uchiyama, T. Honjo, and J. Yodoi. "Origin of human T-lymphotrophic virus I-positive T cell lines in adult T cell leukemia. Analysis of T cell receptor gene rearrangement." Journal of Experimental Medicine 162, no. 6 (December 1, 1985): 2169–74. http://dx.doi.org/10.1084/jem.162.6.2169.

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Using the clone-specific rearrangement of the T cell receptor gene as the genetic marker of the clonotype, we analyzed the clonal origin of the interleukin 2 (IL-2)-dependent human T-lymphotrophic virus I (HTLV-I)-positive T cell lines established from various adult T cell leukemia (ATL) patients. From a patient with chronic ATL, whose leukemic cells proliferated in vitro in response to IL-2, we repeatedly established leukemic T cell clones having the same rearrangement profile of the T beta chain gene as the leukemic cells. By contrast, established cell lines from acute ATL patients had different beta chain gene rearrangements from those of the leukemic cells. These HTLV-I+ T cell lines might not be the direct progeny of the leukemic cells, but that of T cells infected either in vivo or in vitro. These IL-2-reactive nonleukemic T cells might have been selected in vitro, because their leukemic cells failed to respond to IL-2, despite the expression of IL-2 receptor. The analysis of the T cell receptor gene rearrangement may give a new approach for the elucidation of the mechanism of leukemogenesis and the origin of the HTLV-I+ T cell lines in ATL.

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16

Feuer, G., JA Zack, WJ Jr Harrington, R. Valderama, JD Rosenblatt, W. Wachsman, SM Baird, and IS Chen. "Establishment of human T-cell leukemia virus type I T-cell lymphomas in severe combined immunodeficient mice." Blood 82, no. 3 (August 1, 1993): 722–31. http://dx.doi.org/10.1182/blood.v82.3.722.722.

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Abstract Human T-cell leukemia virus type I (HTLV-I) is recognized as the etiologic agent of adult T-cell leukemia (ATL), a disease endemic in certain regions of southeastern Japan, Africa, and the Caribbean basin. Although HTLV-I can immortalize T lymphocytes in culture, factors leading to tumor progression after HTLV-I infection remain elusive. Previous attempts to propagate the ATL tumor cells in animals have been unsuccessful. Severe combined immunodeficient (SCID) mice have previously been used to support the survival of human lymphoid cell populations when inoculated with human peripheral blood lymphocytes (PBL). SCID mice were injected intraperitoneally with PBL from patients diagnosed with ATL, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), or from asymptomatic HTLV-I-seropositive patients. Many of these mice become persistently infected with HTLV-I. Furthermore, after human reconstitution was established in these mice, HTLV-I-infected cells displayed a proliferative advantage over uninfected human cells. Lymphoblastic lymphomas of human origin developed in animals injected with PBL from two ATL patients. The tumor cells represented outgrowth of the original ATL leukemic clone in that they had monoclonal or oligoclonal integrations of the HTLV-I provirus identical to the leukemic clone and predominantly expressed the cell surface markers, CD4 and CD25. In contrast, cell lines derived by HTLV immortalization of T cells in vitro did not persist or form tumors when inoculated into SCID mice, indicating differences between in vitro immortalized cells and ATL leukemic cells. This system represents the first small animal model to study HTLV-I tumorigenesis in vivo.

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17

Feuer, G., JA Zack, WJ Jr Harrington, R. Valderama, JD Rosenblatt, W. Wachsman, SM Baird, and IS Chen. "Establishment of human T-cell leukemia virus type I T-cell lymphomas in severe combined immunodeficient mice." Blood 82, no. 3 (August 1, 1993): 722–31. http://dx.doi.org/10.1182/blood.v82.3.722.bloodjournal823722.

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Human T-cell leukemia virus type I (HTLV-I) is recognized as the etiologic agent of adult T-cell leukemia (ATL), a disease endemic in certain regions of southeastern Japan, Africa, and the Caribbean basin. Although HTLV-I can immortalize T lymphocytes in culture, factors leading to tumor progression after HTLV-I infection remain elusive. Previous attempts to propagate the ATL tumor cells in animals have been unsuccessful. Severe combined immunodeficient (SCID) mice have previously been used to support the survival of human lymphoid cell populations when inoculated with human peripheral blood lymphocytes (PBL). SCID mice were injected intraperitoneally with PBL from patients diagnosed with ATL, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), or from asymptomatic HTLV-I-seropositive patients. Many of these mice become persistently infected with HTLV-I. Furthermore, after human reconstitution was established in these mice, HTLV-I-infected cells displayed a proliferative advantage over uninfected human cells. Lymphoblastic lymphomas of human origin developed in animals injected with PBL from two ATL patients. The tumor cells represented outgrowth of the original ATL leukemic clone in that they had monoclonal or oligoclonal integrations of the HTLV-I provirus identical to the leukemic clone and predominantly expressed the cell surface markers, CD4 and CD25. In contrast, cell lines derived by HTLV immortalization of T cells in vitro did not persist or form tumors when inoculated into SCID mice, indicating differences between in vitro immortalized cells and ATL leukemic cells. This system represents the first small animal model to study HTLV-I tumorigenesis in vivo.

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18

Landmeier, Silke, Bianca Altvater, Sibylle Pscherer, Jutta Meltzer, Josef Vormoor, Juan F. Vera, Martin Pule, Marc Hotfilder, Heribert Juergens, and Claudia Rossig. "CD19-Redirected Cytotoxic T Cells Prevent Engraftment of Primary Human Leukemia Cells In Vivo." Blood 114, no. 22 (November 20, 2009): 3025. http://dx.doi.org/10.1182/blood.v114.22.3025.3025.

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Abstract Abstract 3025 Poster Board II-1001 Due to its restriction to the B-cell lineage and high surface expression in B-cell malignancies, CD19 is an attractive target antigen for immunological strategies in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). While preclinical in vivo studies of CD19-specific cellular immunotherapy have generally used xenografts from human CD19+ leukemia cell lines, primary leukemia cells are likely to more closely mimic the disease in humans and allow to differentiate between standard and high risk situations. Therefore, we investigated the in vivo sensitivity of human leukemic bone marrow to adoptive immunotherapy with gene-modified CD19-specific T cells. Among 15 primary leukemias obtained from the bone marrow of pediatric patients at diagnosis, 10 were successfully engrafted in NOD/scid mice by intrafemoral injection within 6 to 20 weeks. For therapeutic experiments, we focused on one standard risk leukemia, characterized by a rapid and sustained response to multiagent chemotherapy, and on a leukemia bearing the high-risk feature of an MLL rearrangement, which was refractory to standard treatment. Titration experiments demonstrated reliable engraftment of 1×104 leukemic cells per mouse. For CD19-directed T-cell therapy, cytotoxic T cells (CTLs) with native specificity for Epstein-Barr virus antigens were expanded from 4 healthy donors and transduced to express either a codon-optimized CD19-specific chimeric antigen receptor (CAR) containing the intracellular signaling domain of the TCRz chain (CD19-z), or a control CAR directed against the neuroectodermal antigen GD2 (14.G2a-z). Costimulatory domains now commonly used to ensure sustained T-cell activation via CARs were not included, since previous studies have shown that CAR activity in virus-specific CTLs does not benefit from additional signaling elements. CTLs had a uniform CD8+ effector memory T-cell phenotype (CD45RO+, CCR7-), and CAR surface expression was 73±21%, range 32-93% (CD19-z, n=9) and 18±13%, range 6-35% (14.G2a-z, n=5). In vitro cytotoxicity experiments confirmed specific lysis of the CD19+ leukemia cell lines REH (51Cr release 59.7±7.2% at an effector target ratio of 20:1) and SupB15 (66.7±8.6) as well as primary CD19+ leukemic cells from 5 pediatric patients (47.2±13.2%), in the absence of background lysis by 14.G2a-z-transduced control CTLs. 1×104 leukemic cells per mouse from primary engrafted mice were transferred into further cohorts of NOD/scid mice by secondary intrafemoral transplantation, followed by adoptive transfer of 4 doses of 5×106 CTLs via tail vein injection on days 1, 4, 8, and 11. IL-2 (500 IU/mouse) was administered twice-weekly, and sequential murine bone marrow aspirates were analyzed for human leukemia engraftment by flow cytometry using human CD45 and CD19-specific antibodies starting 3 weeks after transplantation. CD19z CTLs prevented engraftment of the standard risk leukemia in 3 of 4 mice, while 3 of 4 control mice developed the leukemia (p = 0.158, Log Rank/Mantel-Cox Test). Moreover, while the MLL-rearranged human leukemia became detectable in the bone marrow of 4 of 5 control mice, followed by overt and fatal leukemia, 5 of 8 mice receiving transfusions of CD19-z transduced CTLs remained disease-free (p = 0.067), and 6 of 8 remained alive, one of them with detectable leukemia cells (p = 0.054) (see Figure). Thus, adoptive transfer of CD19-redirected CTLs efficiently delayed or prevented engraftment of both standard and high risk ALLs in mice and therefore provides a promising treatment option for patients with BCP-ALL refractory to standard treatment. Disclosures No relevant conflicts of interest to declare.

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19

Lauer, Simeon A., Joel Fischer, Joan Jones, Samuel Gartner, Janice Dutcher, and James A. Hoxie. "Orbital T-cell Lymphoma Human T-cell Leukemia Virus-I Infection." Ophthalmology 95, no. 1 (January 1988): 110–15. http://dx.doi.org/10.1016/s0161-6420(88)33231-8.

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20

Kondo, A., K. Imada, T. Hattori, H. Yamabe, T. Tanaka, M. Miyasaka, M. Okuma, and T. Uchiyama. "A model of in vivo cell proliferation of adult T-cell leukemia." Blood 82, no. 8 (October 15, 1993): 2501–9. http://dx.doi.org/10.1182/blood.v82.8.2501.2501.

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Abstract We have made a model of in vivo cell proliferation of leukemic cells from adult T-cell leukemia (ATL) patients using severe combined immunodeficiency (SCID) mice. Peripheral blood mononuclear cells (PBMC) or lymph node cells (LNC) depleted of B cells and monocytes were intraperitoneally injected into SCID mice treated with antimurine interleukin-2 receptor (IL-2+) beta chain monoclonal antibody (MoAb)(TM- beta 1), followed by daily injection of human recombinant IL-2 until 60 days after cell injection. SCID mice injected with ATL cells from 6 of 8 ATL patients were found to have the tumor or leukemia 5 to 7 weeks after the inoculation of cells. Serum levels of soluble form of human IL-2R alpha chain (Tac) were markedly elevated in such mice. The cells recovered from the mice injected with leukemic cells from four different ATL patients had the same cell surface phenotype as that of original leukemic cells which were CD4+Tac+. Furthermore, we detected the same integration site of human T-cell leukemia virus type I (HTLV- I) provirus and the same rearrangement pattern of human T-cell receptor (TCR) beta chain gene as those of ATL cells by Southern blot hybridization, indicating that the cells proliferating in SCID mice were derived from the original ATL cell clone. Histologic examination showed that the pattern of the infiltration of ATL cells into various organs in SCID mice was similar to that of an ATL patient. Such a model of in vivo cell proliferation of ATL cells will be useful for the study of the mechanism of neoplastic cell proliferation and for the development of a new and effective treatment of ATL.

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21

Kondo, A., K. Imada, T. Hattori, H. Yamabe, T. Tanaka, M. Miyasaka, M. Okuma, and T. Uchiyama. "A model of in vivo cell proliferation of adult T-cell leukemia." Blood 82, no. 8 (October 15, 1993): 2501–9. http://dx.doi.org/10.1182/blood.v82.8.2501.bloodjournal8282501.

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We have made a model of in vivo cell proliferation of leukemic cells from adult T-cell leukemia (ATL) patients using severe combined immunodeficiency (SCID) mice. Peripheral blood mononuclear cells (PBMC) or lymph node cells (LNC) depleted of B cells and monocytes were intraperitoneally injected into SCID mice treated with antimurine interleukin-2 receptor (IL-2+) beta chain monoclonal antibody (MoAb)(TM- beta 1), followed by daily injection of human recombinant IL-2 until 60 days after cell injection. SCID mice injected with ATL cells from 6 of 8 ATL patients were found to have the tumor or leukemia 5 to 7 weeks after the inoculation of cells. Serum levels of soluble form of human IL-2R alpha chain (Tac) were markedly elevated in such mice. The cells recovered from the mice injected with leukemic cells from four different ATL patients had the same cell surface phenotype as that of original leukemic cells which were CD4+Tac+. Furthermore, we detected the same integration site of human T-cell leukemia virus type I (HTLV- I) provirus and the same rearrangement pattern of human T-cell receptor (TCR) beta chain gene as those of ATL cells by Southern blot hybridization, indicating that the cells proliferating in SCID mice were derived from the original ATL cell clone. Histologic examination showed that the pattern of the infiltration of ATL cells into various organs in SCID mice was similar to that of an ATL patient. Such a model of in vivo cell proliferation of ATL cells will be useful for the study of the mechanism of neoplastic cell proliferation and for the development of a new and effective treatment of ATL.

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22

Koka, P., K. van de Mark, and D. V. Faller. "trans-Activation of genes encoding activation-associated human T lymphocyte surface proteins by murine retroviral sequences." Journal of Immunology 146, no. 7 (April 1, 1991): 2417–25. http://dx.doi.org/10.4049/jimmunol.146.7.2417.

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Abstract The mechanisms whereby RNA leukemia viruses cause T lymphocyte leukemias or lymphomas after a long latent period are not understood. We report here that infection of human T lymphocyte lines with a murine leukemia virus results in up-regulation of a number of lymphocyte-specific cell surface Ag. These proteins include CD2, CD3, CD4, the TCR, and MHC class I Ag. The expression of other cell surface proteins, such as LFA-3, are unaffected by the presence of the retrovirus. This up-regulation occurs at the level of the mRNA transcripts encoding these proteins, and is the result of increased transcription of the respective genes. The increases in transcription are the result of a trans-activation process by the leukemia virus. The transient introduction of chimeric genes consisting of MHC class I gene promoter sequences attached to the reporter gene CAT into human T cells containing murine retrovirus produces stimulated transcription of the reporter gene. Subgenomic portions of the murine leukemia virus containing the long terminal repeats and the 5' untranslated region are sufficient to produce transactivation of the same set of T cell genes as the whole leukemia virus. The finding that murine leukemia viruses enhance transcription and expression of a group of T cell surface proteins, all of which have been reported to be capable of transducing an activating signal to the lymphocyte, may be relevant to the pathophysiologic mechanisms whereby these viruses induce leukemias and lymphomas.

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23

Kannagi, Mari. "Immunologic Control of Human T-Cell Leukemia Virus Type I and Adult T-Cell Leukemia." International Journal of Hematology 86, no. 2 (August 1, 2007): 113–17. http://dx.doi.org/10.1532/ijh97.07092.

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24

Shimoyama, M., Y. Kagami, K. Shimotohno, M. Miwa, K. Minato, K. Tobinai, K. Suemasu, and T. Sugimura. "Adult T-cell leukemia/lymphoma not associated with human T-cell leukemia virus type I." Proceedings of the National Academy of Sciences 83, no. 12 (June 1, 1986): 4524–28. http://dx.doi.org/10.1073/pnas.83.12.4524.

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25

Larkin, Julie, John T. Sinnott, Joshua Weiss, and Douglas A. Holt. "Human T-Cell Lymphotropic Virus-Type I." Infection Control & Hospital Epidemiology 11, no. 6 (June 1990): 314–18. http://dx.doi.org/10.1086/646177.

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Human T-cell lymphotropic virus type-1 (HTLV-I) is a recently recognized retrovirus identified as the cause of adult T-cell leukemia-lymphoma (ATLL) and HTLV-I-associated myelopathy (TSPI HAM). HTLV-I, a member of theRetroviridaefamily of viruses, was first described in 1980 after the isolation of the virus from a patient with a T-cell lymphoma. These pathogenic retroviruses are typically divided into theOncovirinaeandLentivirinae. The oncovirus group, including HTLV-I, HTLV-II and bovine leukemia virus (BLV), is generally associated with tumors. The lentiviruses are associated with immune deficiency and/or neurologic disease, and include agents such as the visna virus of sheep and the human immunodeficiency virus type-1 and -2 HIV-1 and HIV-2).

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26

Yoshida, M., and M. Seiki. "Human t-cell leukemia virus: Causative roles in development of adult t-cell leukemia and provirus integration into leukemic cell DNA." Hematological Oncology 4, no. 1 (January 1986): 13–20. http://dx.doi.org/10.1002/hon.2900040104.

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27

Franchini, Genoveffa, Risaku Fukumoto, and Jake R. Fullen. "T-Cell Control by Human T-Cell Leukemia/Lymphoma Virus Type 1." International Journal of Hematology 78, no. 4 (November 2003): 280–96. http://dx.doi.org/10.1007/bf02983552.

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28

Waldmann, Thomas A. "Human T-Cell Lymphotropic Virus Type I—Associated Adult T-Cell Leukemia." JAMA 273, no. 9 (March 1, 1995): 735. http://dx.doi.org/10.1001/jama.1995.03520330065039.

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29

Larocca, David, Lorrine A. Chao, Marian H. Seto, and Terence K. Brunck. "Human T-cell Leukemia Virus minus strand transcription in infected T-cells." Biochemical and Biophysical Research Communications 163, no. 2 (September 1989): 1006–13. http://dx.doi.org/10.1016/0006-291x(89)92322-x.

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30

Younis, Ihab,. "The Human T-cell leukemia virus Rex protein." Frontiers in Bioscience 10, no. 1-3 (2005): 431. http://dx.doi.org/10.2741/1539.

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31

Ratner, Lee. "Human T cell lymphotropic virus-associated leukemia/lymphoma." Current Opinion in Oncology 17, no. 5 (September 2005): 469–73. http://dx.doi.org/10.1097/01.cco.0000174037.84903.fb.

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32

Ratner, Lee. "Molecular biology of human T cell leukemia virus." Seminars in Diagnostic Pathology 37, no. 2 (March 2020): 104–9. http://dx.doi.org/10.1053/j.semdp.2019.04.003.

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33

Maehama, T. "Human T cell leukemia virus-1 in pregnancy." International Journal of Gynecology & Obstetrics 87, no. 3 (October 6, 2004): 247–48. http://dx.doi.org/10.1016/j.ijgo.2004.07.024.

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34

Ina, Yasuo, and Takashi Gojobori. "Molecular evolution of human T-cell leukemia virus." Journal of Molecular Evolution 31, no. 6 (December 1990): 493–99. http://dx.doi.org/10.1007/bf02102076.

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35

Yoshie, Osamu, Ryuichi Fujisawa, Takashi Nakayama, Hitomi Harasawa, Hideaki Tago, Dai Izawa, Kunio Hieshima, et al. "Frequent expression of CCR4 in adult T-cell leukemia and human T-cell leukemia virus type 1–transformed T cells." Blood 99, no. 5 (March 1, 2002): 1505–11. http://dx.doi.org/10.1182/blood.v99.5.1505.

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Chemokines and chemokine receptors play important roles in migration and tissue localization of various lymphocyte subsets. Here, we report the highly frequent expression of CCR4 in adult T-cell leukemia (ATL) and human T-cell leukemia virus type 1 (HTLV-1)–immortalized T cells. Flow cytometric analysis revealed that ATL and HTLV-1–immortalized T-cell lines consistently expressed CCR4. Inducible expression of HTLV-1 transcriptional activator tax in a human T-cell line Jurkat did not, however, up-regulate CCR4 mRNA. In vitro immortalization of peripheral blood T cells led to preferential outgrowth of CD4+ T cells expressing CCR4. We further demonstrated highly frequent expression of CCR4 in fresh ATL cells by (1) reverse transcriptase–polymerase chain reaction (RT-PCR) analysis of CCR4 expression in peripheral blood mononuclear cells (PBMCs) from patients with ATL and healthy controls; (2) flow cytometric analysis of CCR4-expressing cells in PBMCs from patients with ATL and healthy controls; (3) CCR4 staining of routine blood smears from patients with ATL; and (4) an efficient migration of fresh ATL cells to the CCR4 ligands, TARC/CCL17 and MDC/CCL22, in chemotaxis assays. Furthermore, we detected strong signals for CCR4, TARC, and MDC in ATL skin lesions by RT-PCR. Collectively, most ATL cases have apparently derived from CD4+ T cells expressing CCR4. It is now known that circulating CCR4+ T cells are mostly polarized to Th2 and also contain essentially all skin-seeking memory T cells. Thus, HTLV-1–infected CCR4+ T cells may have growth advantages by deviating host immune responses to Th2. CCR4 expression may also account for frequent infiltration of ATL into tissues such as skin and lymph nodes.

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Qayyum, Sohail, and John K. Choi. "Adult T-Cell Leukemia/Lymphoma." Archives of Pathology & Laboratory Medicine 138, no. 2 (February 1, 2014): 282–86. http://dx.doi.org/10.5858/arpa.2012-0379-rs.

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Adult T-cell leukemia/lymphoma is a rare mature CD4+ T-cell neoplasm caused by the retrovirus human T-lymphotrophic virus type 1. At present there are approximately 20 million people infected globally with this virus, and most of these individuals belong to the endemic areas in southern Japan, Africa, the Caribbean basin, and Latin America. In the United States, it is usually seen in immigrants from these endemic regions. Adult T-cell leukemia/lymphoma predominantly affects the adult population and is rare in children. Adult T-cell leukemia/lymphoma has 4 subtypes: acute, lymphomatous, chronic, and smoldering. Clinically, the first 2 variants are classified as aggressive, and the latter two are classified as indolent. Given the rare occurrence and diagnostic challenges associated with adult T-cell leukemia/lymphoma, this review will highlight its salient features to aid in recognition of this entity and perform a comprehensive diagnostic workup.

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37

Kawaguchi, Akira, Yasuko Orba, Takashi Kimura, Hidekatsu Iha, Masao Ogata, Takahiro Tsuji, Akira Ainai, et al. "Inhibition of the SDF-1α–CXCR4 axis by the CXCR4 antagonist AMD3100 suppresses the migration of cultured cells from ATL patients and murine lymphoblastoid cells from HTLV-I Tax transgenic mice." Blood 114, no. 14 (October 1, 2009): 2961–68. http://dx.doi.org/10.1182/blood-2008-11-189308.

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Adult T-cell leukemia (ATL) is a T-cell malignancy caused by human T lymphotropic virus type I, and presents as an aggressive leukemia with characteristic widespread leukemic cell infiltration into visceral organs and skin. The molecular mechanisms associated with leukemic cell infiltration are poorly understood. We have used mouse models of ATL to investigate the role of chemokines in this process. Transfer of splenic lymphomatous cells from transgenic to SCID mice reproduces a leukemia and lymphoma that is histologically identical to human disease. It could be shown that lymphomatous cells exhibit specific chemotactic activity in response to stromal cell–derived factor-1α (SDF-1α). Lymphomatous cells exhibited surface expression of CXCR4, the specific receptor of SDF-1α. AMD3100, a CXCR4 antagonist, was found to inhibit both SDF-1α–induced migration and phosphorylation of extracellular signal-related kinase 1/2. Investigation of cultured cells from human ATL patients revealed identical findings. Using the SCID mouse model, it could be demonstrated that AMD3100 inhibited infiltration of lymphomatous cells into liver and lung tissues in vivo. These results demonstrate the involvement of the SDF-1α/CXCR4 interaction as one mechanism of leukemic cell migration and this may provide a novel target as part of combination therapy for ATL.

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38

Koyanagi, Yoshio, Yasuto Itoyama, Naomi Nakamura, Keita Takamatsu, Jun-Ichi Kira, Teruo Iwamasa, Ikuo Goto, and Naoki Yamamoto. "In Vivo Infection of Human T-Cell Leukemia Virus Type I in Non-T Cells." Virology 196, no. 1 (September 1993): 25–33. http://dx.doi.org/10.1006/viro.1993.1451.

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39

Hanai, Shuji, Takayuki Nitta, Momoko Shoda, Masakazu Tanaka, Naomi Iso, Izuru Mizoguchi, Shinji Yashiki, et al. "Integration of human T-cell leukemia virus type 1 in genes of leukemia cells of patients with adult T-cell leukemia." Cancer Science 95, no. 4 (April 2004): 306–10. http://dx.doi.org/10.1111/j.1349-7006.2004.tb03207.x.

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40

Imai, Toshio, Yoshikazu Tanaka, Kenji Fukudome, Shin Takagi, Koichi Araki, and Osamu Yoshie. "Enhanced expression of LFA-3 on human T-cell lines and leukemic cells carrying human T-cell-leukemia virus type 1." International Journal of Cancer 55, no. 5 (November 11, 1993): 811–16. http://dx.doi.org/10.1002/ijc.2910550520.

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41

Mori, Naoki, Takehiro Matsuda, Masayuki Tadano, Takao Kinjo, Yasuaki Yamada, Kunihiro Tsukasaki, Shuichi Ikeda, et al. "Apoptosis Induced by the Histone Deacetylase Inhibitor FR901228 in Human T-Cell Leukemia Virus Type 1-Infected T-Cell Lines and Primary Adult T-Cell Leukemia Cells." Journal of Virology 78, no. 9 (May 1, 2004): 4582–90. http://dx.doi.org/10.1128/jvi.78.9.4582-4590.2004.

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ABSTRACT Inhibition of histone deacetylase (HDAC) activity induces growth arrest, differentiation, and, in certain cell types, apoptosis. FR901228, FK228, or depsipeptide, is an HDAC inhibitor effective in T-cell lymphomas. Adult T-cell leukemia (ATL) is caused by human T-cell leukemia virus type 1 (HTLV-1) and remains incurable. We examined whether FR901228 is effective for treatment of ATL by assessing its ability to induce apoptosis of HTLV-1-infected T-cell lines and primary leukemic cells from ATL patients. FR901228 induced apoptosis of Tax-expressing and -unexpressing HTLV-1-infected T-cell lines and selective apoptosis of primary ATL cells, especially those of patients with acute ATL. FR901228 also efficiently reduced the DNA binding of NF-κB and AP-1 in HTLV-1-infected T-cell lines and primary ATL cells and down-regulated the expression of Bcl-xL and cyclin D2, regulated by NF-κB. Although the viral protein Tax is an activator of NF-κB and AP-1, FR901228-induced apoptosis was not associated with reduced expression of Tax. In vivo use of FR901228 partly inhibited the growth of tumors of HTLV-1-infected T cells transplanted subcutaneously in SCID mice. Our results indicated that FR901228 could induce apoptosis of these cells and suppress the expression of NF-κB and AP-1 and suggest that FR901228 could be therapeutically effective in ATL.

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42

Chorba, TL, R. Brynes, VS Kalyanaraman, M. Telfer, R. Ramsey, A. Mawle, EL Palmer, AT Chen, P. Feorino, and BL Evatt. "Transformed T lymphocytes infected by a novel isolate of human T cell leukemia virus type II." Blood 66, no. 6 (December 1, 1985): 1336–42. http://dx.doi.org/10.1182/blood.v66.6.1336.1336.

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Abstract Human T cell leukemia virus type II (HTLV-II) has been isolated from a patient (Mo) with features of leukemic reticuloendotheliosis (LRE) and from a patient with acquired immunodeficiency syndrome (AIDS). We have obtained another isolate of HTLV-II from a patient (CM) with severe hemophilia A, pancytopenia, and a 14-year history of staphylococcal and candidal infections but no evidence of T cell leukemia/lymphoma, AIDS, or LRE. Fresh mononuclear cells and cultured lymphocytes from CM express retroviral antigens indistinguishable by molecular criteria from HTLV-IIMo. Leukocyte cultures from CM yield hyperdiploid (48,XY, +2, +19) continuous lymphoid lines; human fetal cord blood lymphocytes (CBL) are transformed by cocultivation with these CM cell cultures but retain normal cytogenetic constitution. Electron microscopic examination of the CM cultures and transformed CBL reveals budding of extracellular viral particles, intracellular tubuloreticular structures, and viral particles contained within intracellular vesicles. CM cell cultures and the transformed CBL do not require exogenous interleukin 2, have T cell cytochemical features and mature T helper phenotypes, and exhibit minimal T helper and profound T suppressor activity on pokeweed mitogen-stimulated differentiation of normal B cells. These characteristics, which are similar to those observed with the first HTLV-II isolate, may represent properties of all HTLV-II-infected T cells.

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43

Chorba, TL, R. Brynes, VS Kalyanaraman, M. Telfer, R. Ramsey, A. Mawle, EL Palmer, AT Chen, P. Feorino, and BL Evatt. "Transformed T lymphocytes infected by a novel isolate of human T cell leukemia virus type II." Blood 66, no. 6 (December 1, 1985): 1336–42. http://dx.doi.org/10.1182/blood.v66.6.1336.bloodjournal6661336.

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Human T cell leukemia virus type II (HTLV-II) has been isolated from a patient (Mo) with features of leukemic reticuloendotheliosis (LRE) and from a patient with acquired immunodeficiency syndrome (AIDS). We have obtained another isolate of HTLV-II from a patient (CM) with severe hemophilia A, pancytopenia, and a 14-year history of staphylococcal and candidal infections but no evidence of T cell leukemia/lymphoma, AIDS, or LRE. Fresh mononuclear cells and cultured lymphocytes from CM express retroviral antigens indistinguishable by molecular criteria from HTLV-IIMo. Leukocyte cultures from CM yield hyperdiploid (48,XY, +2, +19) continuous lymphoid lines; human fetal cord blood lymphocytes (CBL) are transformed by cocultivation with these CM cell cultures but retain normal cytogenetic constitution. Electron microscopic examination of the CM cultures and transformed CBL reveals budding of extracellular viral particles, intracellular tubuloreticular structures, and viral particles contained within intracellular vesicles. CM cell cultures and the transformed CBL do not require exogenous interleukin 2, have T cell cytochemical features and mature T helper phenotypes, and exhibit minimal T helper and profound T suppressor activity on pokeweed mitogen-stimulated differentiation of normal B cells. These characteristics, which are similar to those observed with the first HTLV-II isolate, may represent properties of all HTLV-II-infected T cells.

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44

Zhong, Wenbin, Xiuye Cao, Guoping Pan, Qun Niu, Xiaoqin Feng, Mengyang Xu, Mingchuan Li, Yu Huang, Qing Yi, and Daoguang Yan. "ORP4L is a prerequisite for the induction of T-cell leukemogenesis associated with human T-cell leukemia virus 1." Blood 139, no. 7 (February 17, 2022): 1052–65. http://dx.doi.org/10.1182/blood.2021013579.

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Abstract Human T-cell leukemia virus 1 (HTLV-1) causes adult T-cell leukemia (ATL), but the mechanism underlying its initiation remains elusive. In this study, ORP4L was expressed in ATL cells but not in normal T-cells. ORP4L ablation completely blocked T-cell leukemogenesis induced by the HTLV-1 oncoprotein Tax in mice, whereas engineering ORP4L expression in T-cells resulted in T-cell leukemia in mice, suggesting the oncogenic properties and prerequisite of ORP4L promote the initiation of T-cell leukemogenesis. For molecular insight, we found that loss of miR-31 caused by HTLV-1 induced ORP4L expression in T-cells. ORP4L interacts with PI3Kδ to promote PI(3,4,5)P3 generation, contributing to AKT hyperactivation; NF-κB–dependent, p53 inactivation-induced pro-oncogene expression; and T-cell leukemogenesis. Consistently, ORP4L ablation eliminates human ATL cells in patient-derived xenograft ATL models. These results reveal a plausible mechanism of T-cell deterioration by HTLV-1 that can be therapeutically targeted.

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Takahashi, Toshiyuki, Masaya Higuchi, Masaya Fukushi, Masayasu Oie, Masaaki Ito, and Masahiro Fujii. "Homotypic Cell–Cell Adhesion Induced by Human T Cell Leukemia Virus Type 1 Tax Protein in T Cell Lines." Virology 302, no. 1 (October 2002): 132–43. http://dx.doi.org/10.1006/viro.2002.1629.

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46

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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47

Mehta-Shah, Neha, Lee Ratner, and Steven M. Horwitz. "Adult T-Cell Leukemia/Lymphoma." Journal of Oncology Practice 13, no. 8 (August 2017): 487–92. http://dx.doi.org/10.1200/jop.2017.021907.

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Adult T-cell lymphoma/leukemia (ATL) is a rare T-cell lymphoproliferative neoplasm caused by human T-lymphotrophic virus 1. In its more common, aggressive forms, ATL carries one of the poorest prognoses of the non-Hodgkin lymphomas. The disease has clinical subtypes (ie, acute, lymphoma, chronic, and smoldering forms) defined by the presenting features, and therefore, the clinical course can vary. For the smoldering and lower-risk chronic forms, combinations involving antiviral therapies have shown some success. However, in many patients, the more indolent forms will evolve into the more aggressive subtypes. In the more aggressive acute, lymphoma, and higher-risk chronic forms, the literature supports initial treatment with combination chemotherapy followed by allogeneic transplantation as a potentially curative approach. Recently, mogamulizumab and lenalidomide have shown promise in the treatment of ATL. With better understanding of the molecular drivers of this disease, we hope that the therapeutic landscape will continue to expand.

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48

Hall, W. W. "Human T cell lymphotropic virus type I and cutaneous T cell leukemia/lymphoma." Journal of Experimental Medicine 180, no. 5 (November 1, 1994): 1581–85. http://dx.doi.org/10.1084/jem.180.5.1581.

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49

Kinoshita, K., T. Amagasaki, S. Ikeda, J. Suzuyama, K. Toriya, K. Nishino, M. Tagawa, M. Ichimaru, S. Kamihira, and Y. Yamada. "Preleukemic state of adult T cell leukemia: abnormal T lymphocytosis induced by human adult T cell leukemia-lymphoma virus." Blood 66, no. 1 (July 1, 1985): 120–27. http://dx.doi.org/10.1182/blood.v66.1.120.120.

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Abstract We report the clinical, hematologic, and immunologic features of 18 preleukemic adult T cell leukemia (pre-ATL) cases with abnormal T lymphocytosis induced by human adult T cell leukemia-lymphoma virus (HTLV/ATLV). The patients were from the Nagasaki district, which is one of the most endemic areas of ATL in Japan. Pre-ATL is a subclinical T cell abnormality differing from ATL. It is characterized by an insidious onset and appearance of abnormal T lymphocytes (10% to 40%) in the peripheral blood without clinical symptoms except for a few cases transiently presenting fever, skin eruptions, and slight lymphadenopathies. Most abnormal T lymphocytes were small and mature with incised or lobulated nuclei and formed E rosettes with sheep RBCs. Virologic and biomolecular analysis revealed that all cases were infected with HTLV, and proviral DNA was integrated in host lymphocytes from 12 of the 14 cases examined. Furthermore, the lymphocyte populations, including abnormal T lymphocytes, were monoclonal with respect to the site of the provirus integration. Abnormal T lymphocytosis persisted from one to more than seven years in six cases, three of which developed ATL after a one- to five-year pre-ATL stage, whereas abnormal T lymphocytes spontaneously decreased in the other seven patients. However, HTLV-infected monoclonal lymphocytes were detected in four cases examined, even after most of the abnormal T lymphocytes had disappeared. Moreover, the same clonally provirus- integrated lymphocytes persisted in two of four cases not only during the course of abnormal lymphocytosis, but also in the subsequent almost- normal blood. These results indicate that the majority of the cases were in a pre-ATL state with a potential to develop ATL.

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50

Kinoshita, K., T. Amagasaki, S. Ikeda, J. Suzuyama, K. Toriya, K. Nishino, M. Tagawa, M. Ichimaru, S. Kamihira, and Y. Yamada. "Preleukemic state of adult T cell leukemia: abnormal T lymphocytosis induced by human adult T cell leukemia-lymphoma virus." Blood 66, no. 1 (July 1, 1985): 120–27. http://dx.doi.org/10.1182/blood.v66.1.120.bloodjournal661120.

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We report the clinical, hematologic, and immunologic features of 18 preleukemic adult T cell leukemia (pre-ATL) cases with abnormal T lymphocytosis induced by human adult T cell leukemia-lymphoma virus (HTLV/ATLV). The patients were from the Nagasaki district, which is one of the most endemic areas of ATL in Japan. Pre-ATL is a subclinical T cell abnormality differing from ATL. It is characterized by an insidious onset and appearance of abnormal T lymphocytes (10% to 40%) in the peripheral blood without clinical symptoms except for a few cases transiently presenting fever, skin eruptions, and slight lymphadenopathies. Most abnormal T lymphocytes were small and mature with incised or lobulated nuclei and formed E rosettes with sheep RBCs. Virologic and biomolecular analysis revealed that all cases were infected with HTLV, and proviral DNA was integrated in host lymphocytes from 12 of the 14 cases examined. Furthermore, the lymphocyte populations, including abnormal T lymphocytes, were monoclonal with respect to the site of the provirus integration. Abnormal T lymphocytosis persisted from one to more than seven years in six cases, three of which developed ATL after a one- to five-year pre-ATL stage, whereas abnormal T lymphocytes spontaneously decreased in the other seven patients. However, HTLV-infected monoclonal lymphocytes were detected in four cases examined, even after most of the abnormal T lymphocytes had disappeared. Moreover, the same clonally provirus- integrated lymphocytes persisted in two of four cases not only during the course of abnormal lymphocytosis, but also in the subsequent almost- normal blood. These results indicate that the majority of the cases were in a pre-ATL state with a potential to develop ATL.

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