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  • 1
    Electronic Resource
    Electronic Resource
    Induction of interleukin-2 receptor by tumor necrosis factor α on cultured ovarian tumor-associated lymphocytes (1992)
    Springer
    Cancer immunology immunotherapy 35 (1992), S. 83-91 
    Details
    ISSN: 1432-0851
    Keywords: TNFα ; CD8+ CTL ; IL-2R ; TIL/TAL
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have recently reported that autologous tumor-specific cytotoxic T lymphocyte (CTL) lines and clones can be developed from lymphocytes infiltrating ovarian malignant ascites (TAL). In this study, we investigated the biological effects of tumor necrosis factor α (TNFα) in the induction, expansion, long-term proliferation and lytic function of CD8+ TAL. TNFα up-regulated the IL-2 receptor (IL-2R) α chain (Tac antigen) on the surface of CD3+ CD8+ CD4− TAL, enhanced the proliferation of autologous tumor-specific CTL, and potentiated their lytic function in long-term cultures. Furthermore, in the induction and expansion phase of CD8+ TAL, the presence of TNFα was associated with a selective increase in CD8+ IL-2R+ (Tac+) cells, and subsequent decrease in CD4+ IL-2R+ (Tac+) cells. These results suggest that the observed facilitation of the outgrowth of CD8+ cells in TAL cultures may be due, at least in part, to the up-regulation of IL-2R, and indicate the usefulness of TNFα in the analysis of signalling in autologous tumor-reactive CTL.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01741854
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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of receptors for human tumour necrosis factor and their regulation by γ-interferon (1985)
    [s.l.] : Nature Publishing Group
    Nature 318 (1985), S. 665-667 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Fig. 1 SDS-polyacrylamide gel electrophoresis (a) and Mono Q-fast protein liquid chromatography of iodinated TNF-a. (²), The autoradiographs shown in a represent samples from three different iodinations (lanes 1-3). About 10,000 c.p.m. of 125I-TNF were analysed. The Mrs ( x IO3) of protein ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/318665a0
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  • 3
    Electronic Resource
    Electronic Resource
    Human tumour necrosis factor: precursor structure, expression and homology to lymphotoxin (1984)
    [s.l.] : Nature Publishing Group
    Nature 312 (1984), S. 724-729 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Human tumour necrosis factor has about 30% homology in its amino acid sequence with lymphotoxin, a lymphokine that has similar biological properties. Recombinant tumour necrosis factor can be obtained by expression of its complementary DNA in Escherichia coli and induces the haemorrhagic necrosis ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/312724a0
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  • 4
    Electronic Resource
    Electronic Resource
    Cloning and expression of cDNA for human lymphotoxin, a lymphokine with tumour necrosis activity (1984)
    [s.l.] : Nature Publishing Group
    Nature 312 (1984), S. 721-724 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] A chemically-synthesized gene and natural complementary DNA coding for human lymphotoxin were isolated and engineered for expression in Escherichia coli. Purified recombinant lymphotoxin shows cytotoxic activity on murine and human tumour cell lines in vitro and causes necrosis of certain murine ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/312721a0
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  • 5
    Electronic Resource
    Electronic Resource
    TNF-Induced Signaling in Apoptosis (1999)
    Springer
    Journal of clinical immunology 19 (1999), S. 350-364 
    Details
    ISSN: 1573-2592
    Keywords: Tumor necrosis factor ; signaling ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Out of the almost 17 members of the TNF superfamily, TNF is probably the most potent inducer of apoptosis. TNF activates both cell-survival and cell-death mechanisms simultaneously. Activation of NF-kB-dependent genes regulates the survival and proliferative effects pf TNF, whereas activation of caspases regulates the apoptotic effects. TNF-induced apoptosis is mediated primarily through the activation of type I receptors, the death domain of which recruits more than a dozen different signaling proteins, which together are considered part of an apoptotic cascade. This cascade does not, however, account for the role of reactive oxygen intermediates, ceramide, phospholipases, and serine proteases which are also inplicated in TNF-induced apoptosis. This cascade also does not explain how type II TNF receptors which lack the death domain, induce apoptosis. Nevertheless, this review of apoptosis signaling will be limited to those proteins that makeup the cascade.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020546615229
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  • 6
    Electronic Resource
    Electronic Resource
    Suramin inhibits tumor cell cytotoxicity mediated through natural killer cells, lymphokine-activated killer cells, monocytes, and tumor necrosis factor (1994)
    Springer
    Journal of clinical immunology 14 (1994), S. 39-49 
    Details
    ISSN: 1573-2592
    Keywords: Suramin ; tumor cell cytotoxicity ; natural killer cells ; lymphokine-activated killer cells ; monocytes ; tumor necrosis factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Suramin, a polysulfonated naphthylurea, is an antitrypanosomal and antifilarial drug. Because of its anti-reverse transcriptase activity and antiproliferative activity, suramin is also used for the treatment of acquired immunodeficiency syndrome and cancer. In spite of these uses, very little is known about its effects on the immune system. In this report, we investigated the effects of suramin on peripheral blood mononuclear cells. We found that natural killer (NK) cell-mediated cytotoxicity against human erythroblastoid cell line K562 was completely inhibited by suramin in a dose-dependent manner. It also completely blocked lymphokine-activated killer (LAK) cell-mediated cytotoxicity against the human B lymphoblastoid cell lines Raji and Daudi. The cytotoxicity against the human melanoma tumor cell line A-375 mediated by unstimulated and stimulated monocytes was also suppressed by suramin. Maximum inhibition of monocyte-mediated cytotoxicity was observed when suramin was present during both the activation and the effector phases of cytotoxicity. Besides its effects on cell-mediated cytotoxicity, suramin also inhibited the cytotoxic effects of tumor necrosis factor (TNF) against different tumor cell lines. Furthermore, we found that suramin interferes with the binding of TNF with its receptor. Thus our results indicate that suramin overall downregulates the immune system by inhibiting cell-mediated and TNF-mediated cytotoxicity against different tumor cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01541174
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  • 7
    Electronic Resource
    Electronic Resource
    Structure of tumor necrosis factor and its receptor (1991)
    Springer
    Biotherapy 3 (1991), S. 113-120 
    Details
    ISSN: 1573-8280
    Keywords: induction ; lymphotoxin ; physicochemical characteristics ; purification ; receptor ; regulation ; source ; structure ; tumor necrosis factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02172083
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  • 8
    Electronic Resource
    Electronic Resource
    Cell density-dependent regulation of cell surface expression of two types of human tumor necrosis factor receptors and its effect on cellular response (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 54 (1994), S. 453-464 
    Details
    ISSN: 0730-2312
    Keywords: tumor necrosis factor ; protein synthesis ; cell density ; cell proliferation ; receptors ; glutathione ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Tumor necrosis factor (TNF) is a multipotential cytokine known to regulate the growth of a wide variety of normal and tumor cells. It has been shown that the density of cells in culture can modulate the growth regulatory activities of TNF, the mechanism of which, however, is not understood. In this report, we investigated the effect of cell density on the expression of TNF receptors. The receptors were examined on epithelial cells (e.g., HeLa), which primarily express the p60 form, and on myeloid cells (e.g., HL-60) known to express mainly the p80 form. We observed that binding of TNF to both cell lines decreased with increase in cell density. Scatchard analysis of binding on HeLa and HL-60 cells revealed a 4- to 5-fold reduction in the number of TNF receptors without any significant change in receptor affinity in both cell types at high density. The decrease in TNF receptor numbers at high cell density was also observed in several other epithelial and myeloid cell lines. The downmodulation at high cell density was unique to TNF receptors, since minimum change in other cell surface proteins was observed as revealed by fluorescent activated cell sorter analysis. Neutralization of binding with antibodies specific to each type of the receptors revealed that both the p60 and p80 forms of the TNF receptor were equally downmodulated.A decrease in leucine incorporation into proteins was observed with increase in cell density, suggesting a reduction in protein synthesis. Since inhibition of protein synthesis by cycloheximide also leads to a decrease in TNF receptors, it is possible that the density-dependent reduction in TNF receptor number is due to an overall decrease in protein synthesis. The density-dependent decrease in TNF receptors was accompanied by a decrease in intracellular reduced glutathione levels. A reduction in the number of receptors on TNF sensitive tumor cells induced by cell-density correlated with increase in resistance to the cytokine.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240540412
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  • 9
    Electronic Resource
    Electronic Resource
    Effect of cell cycle on the regulation of the cell surface and secreted forms of type I and type II human tumor necrosis factor receptors (1995)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 59 (1995), S. 303-316 
    Details
    ISSN: 0730-2312
    Keywords: TNF ; human histiocytic lymphoma ; protein synthesis ; receptors ; p60 ; p80 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The cell cycle has been shown to regulate the biological effects of human tumor necrosis factor (TNF), but to what extent that regulation is due to the modulation of TNF receptors is not clear. In the present report we investigated the effect of the cell cycle on the expression of surface and soluble TNF receptors in human histiocytic lymphoma U-937. Exposure to hydroxyurea, thymidine, etoposide, bisbensimide, and democolcine lead to accumulation of cells primarily in G1/S, S, S/G2/M, G2/M, and M stages of the cell cycle, respectively. Whilie no significant change in TNF receptors occurred in cells arrested in G1/S or S/G2 stages, about a 50% decrease was observed in cells at M phase of the cycle. Scatchard analysis showed a reduction in receptor number rather than affinity. In contrast, cells arrested at S phase (thymidine) showed an 80% increase in receptor number.The decrease in the TNF receptors was not due to changes in cell size or protein synthesis. The increase in receptors, however, correlated with an increase in total protein synthesis (to 3.8-fold of the control levels). A proportional change was observed in the p60 and p80 forms of the TNF receptors. A decrease in the surface receptors in cells arrested in M phase correlated with an increase in the amount of soluble receptors. The cellular response to TNF increased to 8- and 2-fold in cells arrested in G1 and S phase, respectively; but cells at G2/M phase showed about 6-fold decrease in response. In conclusion, our results demonstrate that the cell cycle plays an important role in regulation of cell-surface and soluble TNF receptors and also in the modulation of cellular response. © 1995 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240590303
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