A human inhibitor of tumor necrosis factor alpha.

Seckinger, P; Isaaz, S; Dayer, Jean‐Michel

doi:10.1084/jem.167.4.1511

Cited by 252 publications

(85 citation statements)

References 9 publications

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“…The soluble forms originating from the extramembranous portion of the TNF-RI (sTNF-RI) and TNF-RII (sTNF-RII) can be found in the culture supernatants of lymphocytes, monocytes and neutrophils [15,[19][20][21] and biological fluids [22,23]. The elevation of sTNF-R in serum/plasma and biological fluids reflecting a variety of inflammatory disorders has been shown in several diseases [24][25][26][27][28][29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Elevation of plasma-soluble tumour necrosis factor receptors (TNF-R) in sarcoidosis

Nakayama

Hashimoto

Amemiya

et al. 1996

Clinical and Experimental Immunology

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SUMMARYTwo types of receptor for tumour necrosis factor-alpha (TNF-R), the 55-kD receptor (TNF-RI) and the 75-kD receptor (TNF-RII), have been identified. Soluble TNF-RI (sTNF-RI) and soluble TNF-RII (sTNF-RII) can be measured in culture supernatants and biological fluids, and the role of sTNF-R has been suggested. In the present study, we measured plasma sTNF-RI and sTNF-RII levels in 19 patients with active sarcoidosis by ELISA in order to assess the state of both types of receptors in this disease. Both plasma sTNF-RI and sTNF-RII levels in patients with active sarcoidosis were significantly higher than those in normal control subjects. A longitudinal evaluation of plasma sTNF-RI and sTNF-RII levels showed that the magnitude of changes in sTNF-RII was closely related with the clinical course of sarcoidosis. These results suggest that plasma sTNF-RII levels may be useful parameters for monitoring the clinical course of sarcoidosis as well as markers for identifying disease activity.

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Section: Introductionmentioning

confidence: 99%

Elevation of plasma-soluble tumour necrosis factor receptors (TNF-R) in sarcoidosis

Nakayama

Hashimoto

Amemiya

et al. 1996

Clinical and Experimental Immunology

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“…UK. urine [13][14][15][16]. Characterization of these inhibitors revealed two immunologically distinct TNF" binding proteins which were shown to be soluble fragments of the extramcmbrane parts of TNF-R [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor soluble receptors behave as acute phase reactants following surgery in patients with rheumatoid arthritis, chronic osteomyelitis and osteoarthritis

Chikanza

Roux‐Lombard

Dayer

et al. 1993

Clinical and Experimental Immunology

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SUMMARY Tumour necrosis factor‐alpha (TNF‐α) is involved in diverse biological processes including immune and inflammatory reactions and the response to surgical stress. Two soluble TNF receptor protein fragments. TNF‐sR55 (from the p55 kD TNF receptor) and TNF‐sR75 (from the p75 kD TNF receptor), are released by cells during inflammation and may modulate the effects of TNF‐α. We have studied the kinetics of secretion of TNF‐α, TNF‐sR55 and TNF‐sR75 in the sera of patients with rheumatoid arthritis (RA) and control subjects with osteoarthritis (OA) or chronic osteomyelitis (OM) before and after major surgery. Significantly higher pre‐operative levels of TNF‐sR55 and TNF‐sR75 were found in RA and OM as compared with OA (P<0.02). Following surgery, TNF‐sR55 increased within 24 h in RA, OM and OA (P<0.05), whereas TNF‐sR75 increased significantly only in OM and OA patients (P<0.05). By contrast, no TNF‐α was detectable before and after surgery in any of the subjects, but this may have been due to impaired detection (by ELISA) of TNF‐α when it is bound to TNF‐sR. These findings suggest that TNF‐sR55 and TNF‐sR75 may be further markers of the host's reaction to inflammatory insults. They may also play a role in modulating the immune and inflammatory reactions by inhibiting the systemic effects of TNF‐α.

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“…Administration of TNF to animals or humans reproduces many of the features of septicemia [5,6]. Recently, naturally occurring inhibitors of TNF activity have been found in the urine of normal individuals and febrile patients and in the serum of patients with renal insufficiency [7][8][9][10][11]. These host mediators, originally termed TNF-binding proteins, have subsequently been identified as the soluble extracellular domains of the 55-and 75-kDa membrane-bound TNF receptors [12][13][14][15][16].…”

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confidence: 99%

Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

Poll

Jansen²,

Leenen³

et al. 1993

Journal of Infectious Diseases

115

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To assess the role of tumor necrosis factor (TNF) in the appearance of soluble TNF receptors (sTNFRs), 20 consecutive patients with a clinical diagnosis of sepsis were studied as were 7 chimpanzees after administration of endotoxin (4 ng/kg) with or without pentoxifylline. The patients had markedly elevated serum levels of sTNFR-p55 and sTNFR-p75 compared with healthy controls (P < .0001 for both receptors). The levels of both soluble receptors correlated with simultaneously measured immunoreactive TNF concentrations (p55: r = .63, P < .01; p75: r = .69, P < .001). In the chimpanzees, endotoxin induced subsequent rises in the serum concentrations ofTNF and sTNFRs. Although pentoxifylline reduced the TNF response to intravenous endotoxin to 20% (P < .05), the appearance of sTNFRs was only moderately inhibited (sTNFRp55 to 79% on average, P < .05; sTNFR-p75 to 77%, P = .12). These results indicate that TNF either does not play an important role in the appearance of sTNFRs in systemic infection or that a small amount of TNF remaining in the circulation after some bacterial challenges is sufficient to preserve the secretion of its soluble receptors.Sepsis is a syndrome characterized by hypotension, vascular leakage, and failure of multiple organs. Tumor necrosis factor (TNF) is an important factor for initiation ofthe septic syndrome [1 ]. Massive induction ofTNF synthesis, resulting in high concentrations of the protein in the circulation, is a prerequisite for the development of shock and multiple organ failure in experimental sepsis in animals [2]. In patients with sepsis, the extent of systemic TNF release correlates strongly with mortality rates [3,4]. Administration of TNF to animals or humans reproduces many of the features of septicemia [5,6]. Recently, naturally occurring inhibitors of TNF activity have been found in the urine of normal individuals and febrile patients and in the serum of patients with renal insufficiency [7][8][9][10][11]. These host mediators, originally termed TNF-binding proteins, have subsequently been identified as the soluble extracellular domains of the 55-and 75-kDa membrane-bound TNF receptors [12][13][14][15][16]. Soluble

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A human inhibitor of tumor necrosis factor alpha.

Cited by 252 publications

References 9 publications

Elevation of plasma-soluble tumour necrosis factor receptors (TNF-R) in sarcoidosis

Elevation of plasma-soluble tumour necrosis factor receptors (TNF-R) in sarcoidosis

Tumour necrosis factor soluble receptors behave as acute phase reactants following surgery in patients with rheumatoid arthritis, chronic osteomyelitis and osteoarthritis

Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

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