Immunochemical characterization of tumor‐associated surface antigens on a moloney leukemia virus‐lymphoma, MBL‐2

Ng, Ah‐Kau; McIntire, K. Robert; Suzuki, Shiro; Aoki, Tadao; Herberman, Ronald B.

doi:10.1002/ijc.2910240420

Cited by 5 publications

(4 citation statements)

References 42 publications

(38 reference statements)

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“…The present results with EL-4(G+) are Compatible with previous data from our laboratory (3) indicating that these cells are susceptible to lysis by primary anti-M-MSV immune cells and can inhibit the cytolysis of RBL-5 or MBL-2 in a cold target inhibition assay. Ng et al (38) also have shown that anti-M-MSV serum lysed EL-4(G+) in the presence of complement. EL-4(G+) cells susceptible to the lysis by the effector cells were shown to contain NB-tropic and xenotropic endogenous type C viruses (39).…”

Section: Discussionmentioning

confidence: 92%

In vitro induction of T-lymphocyte-mediated cytotoxicity by infectious murine type C oncornaviruses.

Taniyama¹,

Holden²

1979

The Journal of Experimental Medicine

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We have developed a system to induce oncornavirus-specific secondary cytotoxic response in vitro. When Moloney strain of murine sarcoma virus-immune spleen cells were cultivated with purified infectious Moloney murine leukemia virus (M-MuLV) or with supernates of tissue culture cells containing infectious virus, a virus-specific secondary cytotoxic response directed against type-specific determinant(s) of M-MuLV was generated in vitro, as determined by a 4-h 51Cr-release assay. The effector cells were susceptible to the treatment with anti-Thyl.2 plus complement, but were unrelated to natural killer cells (NK), because they could not lyse some target cells specific for M-MuLV in both the induction phase and the interaction between effector cells and target cells. Furthermore, a product of the env gene of M-MuLV, perhaps gp70, appeared to be responsible for this response, because viruses with recombinations in the env gene between ecotropic M-MuLV and a xenotropic virus failed to induce a response. When infectious M-MuLV was exposed to UV-light at different doses, the ability of UV-treated M-MuLV to induce a secondary cytotoxic response decreased in parallel with infectivity, indicating that infectivity was necessary for the induction of this response.

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Section: Discussionmentioning

confidence: 92%

In vitro induction of T-lymphocyte-mediated cytotoxicity by infectious murine type C oncornaviruses.

Taniyama¹,

Holden²

1979

The Journal of Experimental Medicine

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“…Parallel experiments were carried out with the MoMLVproducing T lymphoma cell line MBL-2 [30] and with NIH-pSun1 fibroblasts, which express the replication-defective pSun1 virus (Fig. 1), to determine whether hypoxia inhibitory activity on MoMLV-driven genes was also exerted on cell types other than M. As shown in Figure 7, no modulation of the constitutive transcript levels of MoMLV in MBL-2 (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…ANA-1 cell line was established by infection with the J2 recombinant retrovirus and MoMLV. Mannosebinding lectin-2 (MBL-2) cells were derived from a MoMLV-induced T lymphoma [30]. RAW-pEGFP was generated by transfection with the pEGFP-N1 vector.…”

Section: Cell Linesmentioning

confidence: 99%

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Hypoxia inhibits Moloney murine leukemia virus expression in activated macrophages

Puppo

Bosco

Federico

et al. 2006

Journal of Leukocyte Biology

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Hypoxia, a local decrease in oxygen tension, occurring in many pathological processes, modifies macrophage (Mphi) gene expression and function. Here, we provide the first evidence that hypoxia inhibits transgene expression driven by the Moloney murine leukemia virus-long terminal repeats (MoMLV-LTR) in IFN-gamma-activated Mphi. Hypoxia silenced the expression of several MoMLV-LTR-driven genes, including v-myc, enhanced green fluorescence protein, and env, and was effective in different mouse Mphi cell lines and on distinct MoMLV backbone-based viruses. Down-regulation of MoMLV mRNA occurred at the transcriptional level and was associated with decreased retrovirus production, as determined by titration experiments, suggesting that hypoxia may control MoMLV retroviral spread through the suppression of LTR activity. In contrast, genes driven by the CMV or the SV40 promoter were up-regulated or unchanged by hypoxia, indicating a selective inhibitory activity on the MoMLV promoter. It is interesting that hypoxia was ineffective in suppressing MoMLV-LTR-controlled gene expression in T or fibroblast cell lines, suggesting a Mphi lineage-selective action. Finally, we found that MoMLV-mediated gene expression in Mphi was also inhibited by picolinic acid, a tryptophan catabolite with hypoxia-like activity and Mphi-activating properties, suggesting a pathophysiological role of this molecule in viral resistance and its possible use as an antiviral agent.

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The specificity of H‐2‐restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus‐induced tumors II. Altered gp70 display and production of noninfectious virus particles by an insusceptible variant tumor

Green

Brown

1983

Eur J Immunol

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Derived from the susceptible AKR.H-2bSL1 tumor cell line, a variant tumor subclone, cl.18-5, was selectively insusceptible to H-2-restricted anti-AKR/Gross virus cytotoxic T lymphocytes (CTL) due to its failure to be recognized. In this study, the expression of virus-related products by variant cl.18-5 cells was compared to that of AKR.H-2bSL1 cells and a susceptible clone, as an approach towards defining the virus-associated antigens recognized by anti-AKR/Gross virus CTL. Despite the type specificity of the CTL, cl.18-5 displayed normal levels of the group-specific antigen (gag) encoded proteins p30, p15, p12 and p10, and the gag-associated Gross cell surface antigen. These results were confirmed by fluorescence-activated cell sorter analysis employing monoclonal antibodies specific for either AKR p12 or the cell surface glycosylated form of AKR ecotropic gag product. In contrast, cl.18-5 was variably less sensitive than AKR.H-2bSL1 to the action of complement and xenogeneic antisera directed against the envelope (env) product gp70. In addition, a panel of five monoclonal antibodies to gp70, which detect distinct endogenous ecotropic viral determinants, lysed AKR.H-2bSL1, but not cl.18-5 cells. However, absorption experiments indicated that cl.18-5 did express near normal levels of these specificities, suggesting an alteration in the orientation or topographical distribution of these determinants. Consistent with an inappropriate display of env products, cl.18-5 was found to be deficient in the production of infectious ecotropic leukemia virus. The particulate fraction of the cell-free supernatant of cl.18-5 contained normal levels of reverse transcriptase activity, indicating that noninfectious viral particles were being produced. Collectively, these results point to an association between recognition by anti-AKR/Gross virus CTL and the expression of ecotropic gp70 required for infectivity of virus.

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Immunochemical characterization of tumor‐associated surface antigens on a moloney leukemia virus‐lymphoma, MBL‐2

Cited by 5 publications

References 42 publications

In vitro induction of T-lymphocyte-mediated cytotoxicity by infectious murine type C oncornaviruses.

In vitro induction of T-lymphocyte-mediated cytotoxicity by infectious murine type C oncornaviruses.

Hypoxia inhibits Moloney murine leukemia virus expression in activated macrophages

The specificity of H‐2‐restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus‐induced tumors II. Altered gp70 display and production of noninfectious virus particles by an insusceptible variant tumor

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