Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors.

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Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors. / Aderka, D; Engelmann, H; Maor, Y; Brakebusch, C; Wallach, D.

In: Journal of Experimental Medicine, Vol. 175, No. 2, 1992, p. 323-9.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Aderka, D, Engelmann, H, Maor, Y, Brakebusch, C & Wallach, D 1992, 'Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors.', Journal of Experimental Medicine, vol. 175, no. 2, pp. 323-9.

APA

Aderka, D., Engelmann, H., Maor, Y., Brakebusch, C., & Wallach, D. (1992). Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors. Journal of Experimental Medicine, 175(2), 323-9.

Vancouver

Aderka D, Engelmann H, Maor Y, Brakebusch C, Wallach D. Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors. Journal of Experimental Medicine. 1992;175(2):323-9.

Author

Aderka, D ; Engelmann, H ; Maor, Y ; Brakebusch, C ; Wallach, D. / Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors. In: Journal of Experimental Medicine. 1992 ; Vol. 175, No. 2. pp. 323-9.

Bibtex

@article{65fd54a0595b11dd8d9f000ea68e967b,
title = "Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors.",
abstract = "The receptors for tumor necrosis factor (TNF) exist in cell-associated as well as soluble forms, both binding specifically to TNF. Since the soluble forms of TNF receptors (sTNF-Rs) can compete with the cell-associated TNF receptors for TNF, it was suggested that they function as inhibitors of TNF activity; at high concentrations, the sTNF-Rs indeed inhibit TNF effects. However, we report here that in the presence of low concentrations of the sTNF-Rs, effects of TNF whose induction depend on prolonged treatment with this cytokine are augmented, reflecting an attenuation by the sTNF-Rs of spontaneous TNF activity decay. Evidence that this stabilization of TNF activity by the sTNF-Rs follows from stabilization of TNF structure within the complexes that TNF forms with the sTNF-Rs is presented here, suggesting that the sTNF-Rs can affect TNF activity not only by interfering with its binding to cells but also by stabilizing its structure and preserving its activity, thus augmenting some of its effects.",
author = "D Aderka and H Engelmann and Y Maor and C Brakebusch and D Wallach",
note = "Keywords: Cell Count; Cells, Cultured; Chromatography, Gel; Enzyme-Linked Immunosorbent Assay; Fibroblasts; Humans; Kinetics; Leukemia, Lymphocytic, Chronic, B-Cell; Receptors, Cell Surface; Receptors, Tumor Necrosis Factor; Recombinant Proteins; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha",
year = "1992",
language = "English",
volume = "175",
pages = "323--9",
journal = "The Journal of Experimental Medicine",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors.

AU - Aderka, D

AU - Engelmann, H

AU - Maor, Y

AU - Brakebusch, C

AU - Wallach, D

N1 - Keywords: Cell Count; Cells, Cultured; Chromatography, Gel; Enzyme-Linked Immunosorbent Assay; Fibroblasts; Humans; Kinetics; Leukemia, Lymphocytic, Chronic, B-Cell; Receptors, Cell Surface; Receptors, Tumor Necrosis Factor; Recombinant Proteins; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha

PY - 1992

Y1 - 1992

N2 - The receptors for tumor necrosis factor (TNF) exist in cell-associated as well as soluble forms, both binding specifically to TNF. Since the soluble forms of TNF receptors (sTNF-Rs) can compete with the cell-associated TNF receptors for TNF, it was suggested that they function as inhibitors of TNF activity; at high concentrations, the sTNF-Rs indeed inhibit TNF effects. However, we report here that in the presence of low concentrations of the sTNF-Rs, effects of TNF whose induction depend on prolonged treatment with this cytokine are augmented, reflecting an attenuation by the sTNF-Rs of spontaneous TNF activity decay. Evidence that this stabilization of TNF activity by the sTNF-Rs follows from stabilization of TNF structure within the complexes that TNF forms with the sTNF-Rs is presented here, suggesting that the sTNF-Rs can affect TNF activity not only by interfering with its binding to cells but also by stabilizing its structure and preserving its activity, thus augmenting some of its effects.

AB - The receptors for tumor necrosis factor (TNF) exist in cell-associated as well as soluble forms, both binding specifically to TNF. Since the soluble forms of TNF receptors (sTNF-Rs) can compete with the cell-associated TNF receptors for TNF, it was suggested that they function as inhibitors of TNF activity; at high concentrations, the sTNF-Rs indeed inhibit TNF effects. However, we report here that in the presence of low concentrations of the sTNF-Rs, effects of TNF whose induction depend on prolonged treatment with this cytokine are augmented, reflecting an attenuation by the sTNF-Rs of spontaneous TNF activity decay. Evidence that this stabilization of TNF activity by the sTNF-Rs follows from stabilization of TNF structure within the complexes that TNF forms with the sTNF-Rs is presented here, suggesting that the sTNF-Rs can affect TNF activity not only by interfering with its binding to cells but also by stabilizing its structure and preserving its activity, thus augmenting some of its effects.

M3 - Journal article

C2 - 1310100

VL - 175

SP - 323

EP - 329

JO - The Journal of Experimental Medicine

JF - The Journal of Experimental Medicine

SN - 0022-1007

IS - 2

ER -

ID: 5160452