The human T-cell leukemia virus type I Tax protein induces apoptosis which is blocked by the Bcl-2 protein

Yamada, Tomoko; Shoji, Yasuhiro; Goto, Toshiyuki; Nakai, Masuyo; Tsujimoto, Yasuhiro; Hatanaka, Masakazu

doi:10.1128/jvi.68.5.3374-3379.1994

Cited by 126 publications

(44 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ATL is a T-cell neoplasm caused by the human T-cell leukaemia virus type-1 (HTLV-1) the tax gene of which has been implicated in leukaemogenesis (Poiesz et al, 1980). The tax gene product was also shown to lead to reduced susceptibility to apoptosis despite intense expression of Fas-R in cell lines immortalized by HTLV-1 infection (about 2·8fold higher expression than fresh ATL cells) (Yamada et al, 1994). ATL is an aggressive neoplasm for which there is no curative chemotherapy available.…”

Section: Discussionmentioning

confidence: 99%

Quantitative characterization and potential function of membrane Fas/APO‐1 (CD95) receptors on leukaemic cells from chronic B and T lymphoid leukaemias

Kamihira¹,

Yamada²,

Hirakata³

et al. 1997

Br J Haematol

View full text Add to dashboard Cite

Summary.The expression and function of the Fas-receptor (Fas-R) were examined in chronic lymphocytic leukaemia (CLL), hairy cell leukaemia-variant (HCL-v) and adult T-cell leukaemia (ATL). The expression of Fas-R in freshly isolated leukaemic cells was qualitatively and quantitatively different between each disease; faint in B-CLL, moderate in HCL-v and strong in ATL. Both full-length and alternatively spliced truncated forms of Fas mRNA were detected even in CLL B cells with faint to negative Fas-R, and Fas mRNA was also shown to be capable of increasing in vitro expression, i.e. the message was functional. In contrast, Fas-R expression on ATL cells was heterogenous and usually intense with a mean density approximately 3-fold higher than that of normal T cells. Fas-R was confirmed to have the potential function for anti-Fas monoclonal antibody-mediated cell death in vitro in Fas-R þ ATL cells. The expression level of Fas-R on the cells was higher in chronic than acute ATL (10360 v 6260 antibody-binding capacity per cell, mFas ABC ; P < 0·05) and was inversely correlated with serum LDH activity, suggesting that the strong Fas-R accounts for the slow progression of chronic ATL and the negative Fas-R protects from Fasmediated cell death. These results show that Fas-R expression on leukaemic cells is valuable in their characterization and perhaps their function, and may contribute to the progression and immune evasion of malignant clones.

show abstract

Section: Discussionmentioning

confidence: 99%

Quantitative characterization and potential function of membrane Fas/APO‐1 (CD95) receptors on leukaemic cells from chronic B and T lymphoid leukaemias

Kamihira¹,

Yamada²,

Hirakata³

et al. 1997

Br J Haematol

View full text Add to dashboard Cite

show abstract

“…It has been hypothesised that PCD may play a central role in embryonic development, as well as in human malignancies [Smith et al, 1989;Evans, 1993], and in the pathogenesis of several infectious diseases [Zychlinsky, 1993]. In addition, more recently, studies investigating virus-associated lytic processes have been car-ried out and an important role for the apoptotic cell death pathway in numerous viral infections has been found [Desmet, 1988;Ameisen and Capron, 1991;Cohen, 1991;Groux et al, 1991;Hugin et al, 1991;Morey et al, 1993;Takizawa et al, 1993;Hinshaw et al, 1994;Vasconcelos and Lam, 1994;Yamada et al, 1994;Esolen et al, 1995;Tropea et al, 1995;Bagetta et al, 1996;Superti et al, 1996;Mastino et al, 1997]. In particular, different viruses (belonging to various families) have been demonstrated to induce, or to prevent, apoptosis [Jeurissen et al, 1992;McCabe and Orrenius, 1992;Meyaard et al, 1992;Rojko et al, 1992;Thompson, 1995].…”

Section: Introductionmentioning

confidence: 99%

Poliovirus infection induces apoptosis in CaCo-2 cells

et al. 1999

View full text Add to dashboard Cite

The effects of poliovirus infection in CaCo-2 cells, a human enterocyte-like cell line are described. Infected cells were examined by a combination of techniques, including optical and electron microscopy, cytofluorimetric analysis of DNA content, and DNA agarose gel electrophoresis. Results obtained by the different experimental approaches demonstrate that poliovirus infection in enterocyte-like cells can result in an apoptotic process.

show abstract

“…Collective evidence suggests that transactively upregulated TNF-a, through pX expression, could initiate apoptotic death of oligodendrocytes in the early asymptomatic phase of HAM rat disease. Although p4OTax is the main factor linked to induction of apoptotic cell death in HTLV-I infection (14,15), an inhibitory effect was also reported (16).…”

Section: Discussionmentioning

confidence: 98%

Human T‐lymphocyte virus type I (HTLV‐I)‐induced myeloneuropathy in rats: Oligodendrocytes undergo apoptosis in the presence of HTLV‐I

Ohya

Ikeda

Tomaru

et al. 2000

APMIS

View full text Add to dashboard Cite

To investigate the pathogenetic role of human T-lymphocyte virus type I (HTLV-I) in central nervous system disease, a rat model for HTLV-I-associated myelopathy/tropical spastic paraparesis, designated as HAM rat disease, was examined with regard to chronological neuropathology, from early asymptomatic phase to late disease. In the thoracic spinal cord of rats with HTLV-I infection, the first event was the appearance of apoptosis of oligodendrocytes beginning at 7 months after induced infection, thereafter followed by the appearance of white matter degeneration, increase of macrophages/activated microglia and of gemistocytic astrocytes at 12, 15 and 20 months, respectively. In the spinal cord, HTLV-I provirus DNA was evident as early as 4 months after the infection, and HTLV-I pX and the tumor necrosis factor (TNF)-alpha messages began to be expressed at age 7 months, just before or at the same time as the appearance of apoptotic cells. Collective evidence suggests that the apoptotic death of oligodendrocytes, which may be induced either directly by the local expression of HTLV-I or indirectly by TNF-alpha, through the transactive function of p40Tax, is the major cause of chronic progressive myeloneuropathy in Wistar-King-Aptekman-Hokudai rats with HTLV-I infection.

show abstract

The human T-cell leukemia virus type I Tax protein induces apoptosis which is blocked by the Bcl-2 protein

Cited by 126 publications

References 31 publications

Quantitative characterization and potential function of membrane Fas/APO‐1 (CD95) receptors on leukaemic cells from chronic B and T lymphoid leukaemias

Quantitative characterization and potential function of membrane Fas/APO‐1 (CD95) receptors on leukaemic cells from chronic B and T lymphoid leukaemias

Poliovirus infection induces apoptosis in CaCo-2 cells

Human T‐lymphocyte virus type I (HTLV‐I)‐induced myeloneuropathy in rats: Oligodendrocytes undergo apoptosis in the presence of HTLV‐I

Contact Info

Product

Resources

About