scholarly journals Human T-cell leukemia virus type I tax/rex DNA and RNA in cutaneous T- cell lymphoma

Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2663-2671 ◽  
Author(s):  
SK Ghosh ◽  
JT Abrams ◽  
H Terunuma ◽  
EC Vonderheid ◽  
E DeFreitas
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Dna Sequences ◽  
Cell Lymphoma ◽  
Skin Lesions ◽  
T Cell Lymphoma ◽  
Type I ◽  
Cutaneous T Cell Lymphoma ◽  
Cell Leukemia Virus Type ◽  
T Cell Lines

Abstract Peripheral blood mononuclear cells (PBMCs) and T-cell lines from patients with Sezary syndrome (SS) and skin lesions from patients with mycosis fungoides (MF) were examined by polymerase chain reaction (PCR) for DNA sequences homologous to the human retroviruses human T- lymphotropic virus (HTLV)-I and -II. Results obtained using primers and probes from the tax/rex region of HTLV-I indicate that 72% (18/25) of SS patients PBMCs, 80% (20/25) of T-cell lines established from SS- PBMC, and 30% (3/10) of skin lesions from MF patients were positive for HTLV-I tax/rex region DNA. Sequence analysis of the 127-bp fragment amplified by the tax/rex primers from 4 of these individuals was found to be identical to that in prototypic HTLV-I. Negative results were obtained using primers and probes from the HTLV-I gag region and the HTLV-II gag and tax regions. No PCR products were obtained using all primers and probes using DNA from 9 healthy blood donors and 10 cord bloods. Expression of HTLV-I tax/rex mRNA was found in 4 of 8 Sezary patients, as determined by RNA-PCR, indicating that this viral region is being transcribed in vivo. Exposure to Tax/Rex protein in SS- patients is supported by the fact that serum antibodies against p27rex and p40tax was observed in 43% and 29% of these SS patients, respectively. Although the causal relationship between the HTLV-I tax/rex region and cutaneous T-cell lymphoma (CTCL) remains unclear, these findings support the presence of a truncated HTLV-I retrovirus in CTCL patients.

scholarly journals Human T-cell leukemia virus type I tax/rex DNA and RNA in cutaneous T- cell lymphoma

Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2663-2671
Author(s):  
SK Ghosh ◽  
JT Abrams ◽  
H Terunuma ◽  
EC Vonderheid ◽  
E DeFreitas
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Dna Sequences ◽  
Cell Lymphoma ◽  
Skin Lesions ◽  
T Cell Lymphoma ◽  
Type I ◽  
Cutaneous T Cell Lymphoma ◽  
Cell Leukemia Virus Type ◽  
T Cell Lines

Peripheral blood mononuclear cells (PBMCs) and T-cell lines from patients with Sezary syndrome (SS) and skin lesions from patients with mycosis fungoides (MF) were examined by polymerase chain reaction (PCR) for DNA sequences homologous to the human retroviruses human T- lymphotropic virus (HTLV)-I and -II. Results obtained using primers and probes from the tax/rex region of HTLV-I indicate that 72% (18/25) of SS patients PBMCs, 80% (20/25) of T-cell lines established from SS- PBMC, and 30% (3/10) of skin lesions from MF patients were positive for HTLV-I tax/rex region DNA. Sequence analysis of the 127-bp fragment amplified by the tax/rex primers from 4 of these individuals was found to be identical to that in prototypic HTLV-I. Negative results were obtained using primers and probes from the HTLV-I gag region and the HTLV-II gag and tax regions. No PCR products were obtained using all primers and probes using DNA from 9 healthy blood donors and 10 cord bloods. Expression of HTLV-I tax/rex mRNA was found in 4 of 8 Sezary patients, as determined by RNA-PCR, indicating that this viral region is being transcribed in vivo. Exposure to Tax/Rex protein in SS- patients is supported by the fact that serum antibodies against p27rex and p40tax was observed in 43% and 29% of these SS patients, respectively. Although the causal relationship between the HTLV-I tax/rex region and cutaneous T-cell lymphoma (CTCL) remains unclear, these findings support the presence of a truncated HTLV-I retrovirus in CTCL patients.

Short Communication: Deletion of the p16INK4AGene inex VivoAcute Adult T Cell Lymphoma/Leukemia Cells and Methylation of the p16INK4APromoter in HTLV Type I-Infected T Cell Lines

2000 ◽  
Vol 16 (8) ◽  
pp. 709-713 ◽  
Author(s):  
Raffaella Trovato ◽  
Anna Cereseto ◽  
Shigeki Takemoto ◽  
Antoine Gessain ◽  
Toshiki Watanabe ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Short Communication ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Leukemia Cells ◽  
Type I ◽  
T Cell Lines

175 Absence of human T-lymphotropic virus type I in cutaneous T-cell lymphoma

1996 ◽  
Vol 12 (2) ◽  
pp. 211
Author(s):  
A. Kikuchi ◽  
T. Nishikawa ◽  
Y. Ikeda ◽  
K. Yamaguchi
Keyword(s):  
T Cell ◽  
Virus Type ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Type I ◽  
Cutaneous T Cell Lymphoma ◽  
T Lymphotropic Virus

Phototherapy-induced interferon kappa drives type I interferon mediated anticancer responses in cutaneous T cell lymphoma

2021 ◽  
Vol 156 ◽  
pp. S21
Author(s):  
Zizi Yu ◽  
Pablo Vieyra-Garcia ◽  
Theresa Benezeder ◽  
Jack Crouch ◽  
John O’Malley ◽  
...  
Keyword(s):  
T Cell ◽  
Type I Interferon ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Type I ◽  
Cutaneous T Cell Lymphoma

Interleukin-7 and interleukin-15 regulate the expression of thebcl-2 and c-myb genes in cutaneous T-cell lymphoma cells

Blood ◽  
2001 ◽  
Vol 98 (9) ◽  
pp. 2778-2783 ◽  
Author(s):  
Jian-Zhong Qin ◽  
Chun-Lei Zhang ◽  
Jivko Kamarashev ◽  
Reinhard Dummer ◽  
Günter Burg ◽  
...  
Keyword(s):  
Cell Death ◽  
T Cell ◽  
Cell Lymphoma ◽  
Skin Lesions ◽  
Test System ◽  
T Cell Lymphoma ◽  
Cutaneous T Cell Lymphoma ◽  
Interleukin 7 ◽  
Survival Gene ◽  
Myb Genes

Abstract Interleukin-7 (IL-7) and IL-15 have been recently identified as growth factors for cutaneous T-cell lymphoma (CTCL) cells, and they protect these cells from cell death. Using the CTCL cell line SeAx as a test system now shows that IL-7 and IL-15 are indeed necessary to maintain high levels of bcl-2. The up-regulation of bcl-2 was paralleled by increased DNA-binding activities of the transcription factors STAT2, STAT5, STAT6, and c-Myb to bcl-2gene promoter–enhancer elements. Because STAT5 and c-Myb positively regulate bcl-2, IL-7 and IL-15 may mediate some of their effects on cell death survival gene expression through these 2 factors. Constitutive activities of the 3 STAT factors and c-Myb were found in the IL-7– and IL-15–independent CTCL cell lines HUT78 and MyLa 2059. The c-Myb protein was also present in CTCL cells of the skin lesions of all investigated patients. These results indicate that IL-7 and IL-15 may increase bcl-2 expression in CTCL cells by the activation of c-myb and STAT factors.

scholarly journals Curcumin Selectively Induces Apoptosis in Cutaneous T-Cell Lymphoma Cell Lines and Patients’ PBMCs: Potential Role for STAT-3 and NF-κB Signaling

2010 ◽  
Vol 130 (8) ◽  
pp. 2110-2119 ◽  
Author(s):  
Chunlei Zhang ◽  
Baoqiang Li ◽  
Xiang Zhang ◽  
Parul Hazarika ◽  
Bharat B. Aggarwal ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Potential Role ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Lymphoma Cell ◽  
Cutaneous T Cell Lymphoma

Suppression of Cell Growth and Induction of Apoptosis of HTLV-I-Infected T-Cell Lines and Primary ATL Cells by Galectin-9.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4810-4810
Author(s):  
Taeko Okudaira ◽  
Mariko Tomita ◽  
Mitsuomi Hirashima ◽  
Naoki Mori
Keyword(s):  
T Cell ◽  
Cell Growth ◽  
Cell Lines ◽  
Cyclin B1 ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Galectin 3 ◽  
T Cell Lines

Abstract Adult T-cell leukemia (ATL) is a fatal malignancy of T lymphocytes caused by infection with human T-cell leukemia virus type I (HTLV-I), and remains incurable. Therefore, novel treatments are urgently needed. Galectins are a family of animal lectins with diverse biological activities. They function both extracellularly, by interacting with cell-surface and extracellular matrix glycoproteins and glycolipids, and intracellularly, by interacting with cytoplasmic and nuclear proteins to modulate signaling pathways. The distribution of galectins is quite diverse, and their expression in various leukocytes has been observed. To determine whether expression of galectins in T cells correlates with HTLV-I infection, we surveyed a number of uninfected and HTLV-I-infected T-cell lines for galectin-3, -8, and -9 expression by RT-PCR. Expression of galectin-8 did not correlate with HTLV-I infection. Galectin-3 was abundantly expressed in HTLV-I-infected T-cell lines and primary ATL cells, but not in uninfected T-cell lines. In contrast, galectin-9 was abundantly expressed in uninfected T-cell lines and normal PBMCs, but not in HTLV-I-infected T-cell lines and primary ATL cells. HTLV-I transformed protein, Tax, did not affect the expression of galectin-3 and -9. It was previously shown that galectin-8 and -9 are proapoptotic proteins. We found that galectin-9 prevented cell growth of HTLV-I-infected T-cell lines and primary ATL cells compared with galectin-8. Galectin-9 induced cell cycle arrest by reducing the expression of cyclin D1, cyclin D2, cyclin B1, Cdk1, Cdk4, Cdk6, and Cdc25C, and apoptosis by reducing the expression of XIAP and c-IAP2. Most of these genes are known to be regulated by NF-κB, which plays a critical role in oncogenesis by HTLV-I. Galectin-9 suppressed phosphorylation of IκBα. Most importantly, treatment with galectin-9 reduced tumor formation from an HTLV-I-infected T-cell line, HUT-102, when these cells were inoculated s.c. into severe combined immunodeficient mice. Our results suggest that galectin-9 may be a new approach for management of ATL.

Human T-Cell Leukemia Virus Type I Tax Activates CD69 Gene Expression.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2256-2256
Author(s):  
Chie Ishikawa ◽  
Taeko Okudaira ◽  
Tetsuro Nakazato ◽  
Mariko Tomita ◽  
Naoki Mori
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Leukemia Virus ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cell Leukemia Virus Type ◽  
Human T Cell ◽  
Cd69 Expression ◽  
T Cell Lines

Abstract The human T-cell leukemia virus type I (HTLV-I) is an oncogenic retrovirus that is etiologically linked to the genesis of adult T-cell leukemia (ATL). Emerging evidence suggests that the pathogenicity of ATL involves suppression of the overall immune response, although the underlying mechanism remains unclear. In this study, we demonstrated that HTLV-I transactivator Tax induces the aberrant expression of CD69, an early leukocyte activation molecule that plays an important role in downregulation of the immune response. In a panel of HTLV-I-infected T-cell lines, CD69 expression was highly elevated compared to HTLV-I-negative T-cell lines at both mRNA and protein levels. Furthermore, CD69 expression correlated with Tax expression. Peripheral blood mononuclear cells from ATL patients also showed an increased expression of CD69 compared with controls. In vitro infection of a T-cell line with HTLV-I was associated with CD69 expression in conjunction with the increasing Tax expression. Expression of CD69 was dependent upon Tax expression in the inducible Tax-expressing cell line JPX-9. Tax transactivated the CD69 gene promoter in a transient transfection assay. Using Tax mutants and dominant negative mutants of IκBs, IKKs, NIK, and CREB, we demonstrated that Tax-induced CD69 expression required the NF-κB and CREB signaling pathways. A series of deletion and mutation analyses of the CD69 gene promoter indicated that two NF-κB, two EGR, and a CRE sequences were critical for Tax transactivation. Electrophoretic mobility shift assay showed the formation of specific protein-DNA complexes in HTLV-I-infected T-cell lines. These results suggest that Tax directly transactivated CD69 gene expression, through multiple cis-acting elements and by the interplay of transcription factors of the NF-κB, EGR, and CREB families. Tax-induced CD69 expression may be involved in immune suppression in ATL.

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