Prevention of Adult T-Cell Leukemia-Like Lymphoproliferative Disease in Rats by Adoptively Transferred T Cells from a Donor Immunized with Human T-Cell Leukemia Virus Type 1 Tax-Coding DNA Vaccine

Ohashi, Takashi; Hanabuchi, Shino; Kato, Hirotomo; Tateno, Hiromi; Takemura, Fumiyo; Tsukahara, Tomonori; Koya, Yoshihiro; Hasegawa, Atsuhiko; Masuda, Tohru; Kannagi, Mari

doi:10.1128/jvi.74.20.9610-9616.2000

Cited by 71 publications

(58 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One suggestion has been the vaccination of HTLV-I carriers with high proviral load and low HTLV-specific T-cell responses with a HTLV-I Taxtargeted vaccine . ATLL-like lymphoproliferative disease in rats has been prevented by adoptive transfer of T cells immunized with HTLV-I Tax DNA (Ohashi et al, 2000). This is analogous to the control of post-transplantation EBV-associated lymphoproliferation by reducing immune suppression or by infusion of EBV-specific CTL.…”

Section: Prevention Of Atllmentioning

confidence: 83%

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

2005

View full text Add to dashboard Cite

After cell-to-cell transmission, HTLV-I increases its viral genome by de novo infection and proliferation of infected cells. Proliferation of infected cells is clonal and persistent in vivo. During the carrier state, infected cells are selected in vivo by the host's immune system, the genetic and epigenetic environment of proviral integration sites, and other factors. In leukemic cells, tax gene expression is frequently impaired by genetic and epigenetic mechanisms. Such loss of Tax expression enables ATL cells to escape the host immune system. On the other hand, ATL cells acquire the ability to proliferate without Tax by intracellular genetic and epigenetic changes. Despite advances in support and the development of novel treatment agents, the prognosis for ATLL remains poor. A number of therapies, however, do appear to improve prognosis compared to CHOP (VEPA). These include interferon-a plus zidovudine (probably after 1-2 cycles of CHOP), intensive chemotherapy as in LSG-15 with G-CSF support and Allo-SCT (which includes the potential for cure). Emerging novel approaches include HDAC inhibitors, monoclonal antibodies, and proteasome inhibitors. Comparison between different therapeutic approaches is complicated by the range of natural history of ATLL, different recruitments of naı¨ve-to-therapy, refractory or relapsed patients, and variations in the reporting of outcome that frequently excludes difficultto-evaluate patients. Moreover, results from relatively small proof-of-principle studies have not been extended with randomized, controlled trials. As a result, currently, there is no clear evidence to support the value of any particular treatment approach over others. To avoid further unnecessary patient suffering and to identify optimal therapy as rapidly as possible, large randomized, controlled trials encompassing multicenter, international collaborations will be necessary.

show abstract

Section: Prevention Of Atllmentioning

confidence: 83%

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

2005

View full text Add to dashboard Cite

show abstract

“…14 Immunization was carried out 3 times with a 1-week interval. One week after final immunization, rats were sacrificed and spleen cells were collected.…”

Section: Dna-vaccination To Ratsmentioning

confidence: 99%

“…12,13 Vaccination with autologous HTLV-I-infected cells, 12 Tax-encoding DNA, 14 or oligopeptides corresponding to a CTL-epitope 15 elicited antitumor effects in this model. HTLV-I Tax serves as an immunodominant target antigen for HTLV-I-specific CTL not only in rats but also in humans.…”

mentioning

confidence: 99%

Potential immunogenicity of adult T cell leukemia cells in vivo

Kurihara

Harashima

Hanabuchi

et al. 2004

Intl Journal of Cancer

Self Cite

View full text Add to dashboard Cite

show abstract

“…The defect, which is probably situated at the level of Rex and protease activities, could be overcome by replacement of the env gene with the corresponding envelope sequence of an ecotropic Moloney murine leukemia virus (Delebecque et al, 2002). Transgenics and direct HTLV infection in rats yielded various pathologies (thymoma, chronic destructive arthritis) and made it possible to evaluate the immune response (cytotoxic activity, involvement of major histocompatibility complex class I downregulation), to assess therapeutic strategies (vaccination, adoptive transfer) and to test the routes of infection (Kazanji et al, 1997a;Ohashi et al, 2000Ohashi et al, , 2002Hanabuchi et al, 2001;Nakamaru et al, 2001;Kikuchi et al, 2002;Sugaya et al, 2002;Hasegawa et al, 2003). A major contribution of another species, the rabbit, was the identification of viral genetic determinants required for HTLV-1 infectivity and pathogenesis (Leno et al, 1995;Collins et al, 1998;Simpson et al, 1998;Bartoe et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Reduced cell turnover in lymphocytic monkeys infected by human T-lymphotropic virus type 1

et al. 2005

View full text Add to dashboard Cite

Understanding cell dynamics in animal models have implications for therapeutic strategies elaborated against leukemia in human. Quantification of the cell turnover in closely related primate systems is particularly important for rare and aggressive forms of human cancers, such as adult T-cell leukemia. For this purpose, we have measured the death and proliferation rates of the CD4 þ T lymphocyte population in squirrel monkeys (Saimiri sciureus) infected by human T-lymphotropic virus type 1 (HTLV-1). The kinetics of in vivo bromodeoxyuridine labeling revealed no modulation of the cell turnover in HTLV-1-infected monkeys with normal CD4 cell counts. In contrast, a substantial decrease in the proliferation rate of the CD4 þ T population was observed in lymphocytic monkeys (e.g. characterized by excessive proportions of CD4 þ T lymphocytes and by the presence of abnormal flower-like cells). Unexpectedly, onset of HTLV-associated leukemia thus occurs in the absence of increased CD4 þ T-cell proliferation. This dynamics significantly differs from the generalized activation of the T-cell turnover induced by other primate lymphotropic viruses like HIV and SIV.

show abstract

Prevention of Adult T-Cell Leukemia-Like Lymphoproliferative Disease in Rats by Adoptively Transferred T Cells from a Donor Immunized with Human T-Cell Leukemia Virus Type 1 Tax-Coding DNA Vaccine

Abstract: Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) in infected individuals

Cited by 71 publications

References 51 publications

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

Potential immunogenicity of adult T cell leukemia cells in vivo

Reduced cell turnover in lymphocytic monkeys infected by human T-lymphotropic virus type 1

Contact Info

Product

Resources

About