A new class of murine leukemia virus associated with development of spontaneous lymphomas.

Hartley, Janet W.; Wolford, Nancy K.; Old, Lloyd J.; Rowe, Wallace P.

doi:10.1073/pnas.74.2.789

Cited by 604 publications

(471 citation statements)

References 23 publications

Supporting

Mentioning

462

Contrasting

Unclassified

Order By: Relevance

“…MCF viruses were isolated from mice by plating mitomycin Ctreated lymphoid cells as infectious centers onto mink lung (ATCC CCL-64) or SC-1 (16) cells as described previously (9). The viruses were adapted to cell-free passage in mink lung cell cultures and were carried through two cycles of limiting dilution purification.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses.

Cloyd

Hartley

Rowe

1980

The Journal of Experimental Medicine

Self Cite

298

219

View full text Add to dashboard Cite

Recombinant mink cell focus-inducing (MCF) murine leukemic viruses, as well as ecotropic and xenotropic viruses, were tested for ability to accelerate or cause development of lymphoma in AKR and other strains of mice. Of the three classes of virus isolated from AKR, only the MCF viruses were able to accelerate development of AKR lymphoma. This fully supports the idea that the MCF viruses are the proximal cause of spontaneous AKR lymphoma. MCF lymphomagenicity was strain specific, however, in that AKR MCF viruses did not induce lymphomas in many murine strains; they were moderately lymphomagenic in C3H/Bi mice and in National Institutes of Health Swiss partially congenic for Akv-1 or Akv-2. In contrast, MCF viruses from nonthymic hematopoietic neoplasms of C3H/Fg, BALB/c, or mice partially congenic for ecotropic virus loci (Akv-1, Akv-2, Fgv-1, C58v-1, and C58v-2) were not able to accelerate or cause lymphomia in AKR or any other mouse strain tested, including some of the strains of origin. MCF lymphomagenicity correlated with thymic origin in the virus and with ability to replicate in the thymus.

show abstract

Section: Methodsmentioning

confidence: 99%

“…Xenotropic and wild mouse amphotropic viruses were titrated on mink S+L -cells (19). MCF viruses were quantitated by focus-formation in mink lung cells (9). NT, not tested.…”

Section: Methodsmentioning

confidence: 99%

Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses.

Cloyd

Hartley

Rowe

1980

The Journal of Experimental Medicine

Self Cite

298

219

View full text Add to dashboard Cite

show abstract

“…Thus, it was found that response to CT26, MC38, A20 and NS1 was significantly higher that that observed for P815 or 18Neo ( p Ͻ 0.05). Because the MuLV gp70 env transcript is expressed in a variety of tumor cells and has been described as a tumor Ag (18,(25)(26)(27), we tested the presence of gp70 RNA transcripts in the different cell lines by RT-PCR. As shown in Fig.…”

Section: Cd4 ϩ Cells Induced In the Absence Of Cd25 ϩ And Cd8 ϩ Cellmentioning

confidence: 99%

CD4+/CD25+ Regulatory Cells Inhibit Activation of Tumor-Primed CD4+ T Cells with IFN-γ-Dependent Antiangiogenic Activity, as well as Long-Lasting Tumor Immunity Elicited by Peptide Vaccination

Casares

Arribillaga

Sarobe

et al. 2003

The Journal of Immunology

193

147

View full text Add to dashboard Cite

CD25+ regulatory T (T reg) cells suppress the activation/proliferation of other CD4+ or CD8+ T cells in vitro. Also, down-regulation of CD25+ T reg cells enhance antitumor immune responses. In this study, we show that depletion of CD25+ T reg cells allows the host to induce both CD4+ and CD8+ antitumoral responses following tumor challenge. Simultaneous depletion of CD25+ and CD8+ cells, as well as adoptive transfer experiments, revealed that tumor-specific CD4+ T cells, which emerged in the absence of CD25+ T reg cells, were able to reject CT26 colon cancer cells, a MHC class II-negative tumor. The antitumoral effect mediated by CD4+ T cells was dependent on IFN-γ production, which exerted a potent antiangiogenic activity. The capacity of the host to mount this antitumor response is lost once the number of CD25+ T reg cells is restored over time. However, CD25+ T reg cell depletion before immunization with AH1 (a cytotoxic T cell determinant from CT26 tumor cells) permits the induction of a long-lasting antitumoral immune response, not observed if immunization is conducted in the presence of regulatory cells. A study of the effect of different levels of depletion of CD25+ T reg cells before immunization with the peptide AH1 alone, or in combination with a Th determinant, unraveled that Th cells play an important role in overcoming the suppressive effect of CD25+ T reg on the induction of long-lasting cellular immune responses.

show abstract

“…Although the AKR/J strain has the predisposition to develop the disease since birth [4], the mean latent period is delayed until the age of 8 months. The long latent period has been attributed to the delayed formation of the leukemogenic dual tropic virus (DTV) with the MCF characteristic [5,6], formed in the thymus as a consequence of recombination within the envelope gene of ecotropic and xenotropic murine leukemia virus (MuLV). DTVs are detected only in preleukemic thymus and leukemic tissues of strains of mice prone to develop high incidence of leukemia [7].…”

mentioning

confidence: 99%

Intervention in Potential Leukemic Cell Migration Pathway Affects Leukemogenesis

Peled

Haran-Ghera

1989

Haematology and Blood Transfusion / Hämatologie Und Bluttransfusion

View full text Add to dashboard Cite

A new class of murine leukemia virus associated with development of spontaneous lymphomas.

Abstract: A new type of murine leukemia virus has been detected in thymuses of eukemic and late preleukemic AKR mice, in lymphomas developing in NIH Swiss mice carrying the AKR ecotropic virus-inducing loci Akv-1 or Akv-2, and in

Cited by 604 publications

References 23 publications

Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses.

Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses.

CD4+/CD25+ Regulatory Cells Inhibit Activation of Tumor-Primed CD4+ T Cells with IFN-γ-Dependent Antiangiogenic Activity, as well as Long-Lasting Tumor Immunity Elicited by Peptide Vaccination

Intervention in Potential Leukemic Cell Migration Pathway Affects Leukemogenesis

Contact Info

Product

Resources

About