A tumor necrosis factor binding protein is present in human biological fluids (original) (raw)
2009, European Journal of Haematology
AI-generated Abstract
This study explores the presence of a tumor necrosis factor binding protein (TNF-BP) in human biological fluids, particularly in the urine of patients undergoing regular hemodialysis. The research highlights the regulatory role of TNF-BP on the biological activity of tumor necrosis factor (TNF), a cytokine involved in inflammation and immunity. The findings suggest that TNF-BP has the potential to serve as a therapeutic agent against TNF-related pathologies, such as septic shock.
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Tumor necrosis factor (TNFα) binding protein: Interference in immunoassays of TNFα
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Journal of Clinical Investigation, 1992
Serial plasma samples from human volunteers obtained after intravenous administration of Escherichia coli endotoxin were analyzed for the presence of circulating soluble tumor necrosis factor receptors (sTNFR). A fourto fivefold increase of type A (p75) and type B (p55) sTNFR was observed 3 h after endotoxin challenge. Pretreatment of the volunteers with ibuprofen before the injection of endotoxin resulted in a slight increase (3.87±0.2 vs. 3.27±03 ng/ml) and temporal shift of sTNFR-A release concurrent to a marked augmentation of TNF levels (603±118 vs. 338±56 pg/nml) as compared to the group without ibuprofen pretreatment. There was a significant correlation between peak sTNFR-A levels and peak TNF levels in the individual probands (r = 0.52, P = 0.04). On the contrary, release kinetics and plasma concentrations of sTNFR-B were identical in both groups (738±0.69 vs. 7.44±033 ng/ml) and no correlation with individual TNF levels was observed. The amount of sTNFR liberated upon endotoxin challenge was not sufficient to block TNF-mediated cytotoxic effects. Our data indicate that the release in vivo of type A and type B sTNFR upon a short exposure to endotoxin is regulated differently. (J. Clin. Invest. 1992. 90:533-536.) Key words: lipopolysaccharide * tumor necrosis factor-binding protein * human * ibuprofen * cyclooxygenase inhibitor Significant amounts of proteins that inhibit TNF activity, termed TNF-binding proteins, have been detected in febrile patients (4), in patients undergoing hemodialysis (5)
Tumor necrosis factor Characterization at the molecular, cellular and in vivo level
Febs Letters, 1991
TNF was originally characterized as an antitumor agent and a factor cytotoxic for many malignant cells. It is now clear that it plays an important role in the defense against viral, bacterial and parasitic infections, -and in (auto-)immune responses. Natural induction of TWF is protective, but its overproduction may he detrimental and even lethal to the host. The steucture of TNF and its interaction with the two types of cellular receptor are becoming better understood. TNF elicits a variety of events in different cell types. It subverts the electron transport system or the mitochondria into production of oxygen radicals, which can kill the (malignant) cells when these do not contain or produce protective enzymes. Furthermore, TNF induces a set of genes and at least part of this transcriptional activation is mediated by NFKB. The prospects of TNF as an antitumor drug can be improved on the one hand by agents such as LI+, which synergizes, and on the other hand by inhibitors of the systemic toxicity which do not interfere with the antitumor efficacy. Also, in tumor-bearing animals which have been rendered tolerant by administration of small doses of TNF, an effective and complete elimination of the tumors can be obtained by the combined action of TNF plus interferon.
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