Isolation and characterization of eight tumor necrosis factor-induced gene sequences from human fibroblasts.

Lee, Tae Hee; Lee, Gene W.; Ziff, Edward B.; Vilček, Ján

doi:10.1128/mcb.10.5.1982

Cited by 149 publications

(124 citation statements)

References 45 publications

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“…Similar to the GCP-2 induction, the IL-8 production induced by TNF-␣ was decreased by IFN-␥. These findings confirm the previously observed inhibition of TNF-␣-induced IL-8 mRNA expression by IFN-␤ and IFN-␥ in fibroblasts (Lee et al, 1990;Oliveira et al, 1992). Furthermore, IFN-␥ has been shown to inhibit TNF-␣-induced IL-8 production in endothelial cells (Nyhlén et al, 2000).…”

Section: Regulation Of Gcp-2 In Connective Tissuesupporting

confidence: 91%

The CXC Chemokine GCP-2/CXCL6 Is Predominantly Induced in Mesenchymal Cells by Interleukin-1β and Is Down-Regulated by Interferon-γ: Comparison with Interleukin-8/CXCL8

Wuyts

Struyf

Gijsbers

et al. 2003

Laboratory Investigation

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SUMMARY:Human granulocyte chemotactic protein-2 (GCP-2)/CXCL6 is a CXC chemokine that functionally uses both of the IL-8/CXCL8 receptors to chemoattract neutrophils but that is structurally most related to epithelial cell-derived neutrophil attractant-78 (ENA-78)/CXCL5. This study provides the first evidence that GCP-2 protein is, compared with IL-8, weakly produced by some sarcoma, but less by carcinoma cells, and is tightly regulated in normal mesenchymal cells. IL-1␤ was the predominant GCP-2 inducer in fibroblasts, chondrocytes, and endothelial cells, whereas IL-8 was equally well up-regulated in these cells by TNF-␣, measles virus, or double-stranded RNA (dsRNA). In contrast, lipopolysaccharide (LPS) was a relatively better stimulus for GCP-2 versus IL-8 in fibroblasts. IFN-␥ down-regulated the GCP-2 production in fibroblasts induced by IL-1␤, TNF-␣, LPS, or dsRNA. The kinetics of GCP-2 induction by IL-1␤, LPS, or dsRNA in fibroblasts differed from those of IL-8. Freshly isolated peripheral blood mononuclear leukocytes, which are a good source of IL-8 and ENA-78, failed to produce GCP-2. However, lung macrophages and blood monocyte-derived macrophages produced GCP-2 in response to LPS. Quantitatively, secretion of GCP-2 always remained inferior to that of IL-8, despite the fact that the ELISA recognized all posttranslationally modified GCP-2 isoforms. The expression of GCP-2 was confirmed in vivo by immunohistochemistry. The patterns of producer cell types, inducers and kinetics and the quantities of GCP-2 produced, suggest a unique role for GCP-2 in physiologic and pathologic processes. (Lab Invest 2003, 83:23-34).

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Section: Regulation Of Gcp-2 In Connective Tissuesupporting

confidence: 91%

The CXC Chemokine GCP-2/CXCL6 Is Predominantly Induced in Mesenchymal Cells by Interleukin-1β and Is Down-Regulated by Interferon-γ: Comparison with Interleukin-8/CXCL8

Wuyts

Struyf

Gijsbers

et al. 2003

Laboratory Investigation

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“…Tumor necrosis factor (TNF)-stimulated gene 14 , encoding a 45-kDa secreted glycoprotein, was originally cloned from normal human fibroblasts stimulated with TNF [1][2][3]. The same gene has been cloned from interleukin-1 (IL-1)-treated human vascular endothelial cells and named PTX3 [4].…”

Section: Introductionmentioning

confidence: 99%

Differential regulation of TSG-14 expression in murine fibroblasts and peritoneal macrophages

Goodman

Levy

Reis

et al. 2000

Journal of Leukocyte Biology

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“…Tumor necrosis factor ␣ (TNF␣)-induced protein 6 (Tnfip6), the secreted product of TNF␣-stimulated gene 6 (TSG-6), is a member of the hyaladherin superfamily of hyaluronan (HA) binding proteins (1,2). The constitutive expression of Tnfip6 is very low, but virtually all cell types of mesenchyme origin can produce Tnfip6 in response to proinflammatory stimuli (2)(3)(4)(5).…”

mentioning

confidence: 99%

Enhanced neutrophil extravasation and rapid progression of proteoglycan‐induced arthritis in TSG‐6–knockout mice

Szántó¹,

Bárdos²,

Gál³

et al. 2004

Arthritis & Rheumatism

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Objective. To gain insight into the mechanisms of the antiinflammatory effect of tumor necrosis factor ␣ (TNF␣)-induced protein 6 (Tnfip6) in arthritis, using Tnfip6-deficient animals.Methods. TNF␣-stimulated gene 6 (TSG-6) coding for Tnfip6 was disrupted. Tnfip6-deficient mice were backcrossed into proteoglycan-induced arthritis (PGIA)-susceptible BALB/c mice, and arthritis was induced by systemic immunization with cartilage proteoglycan (PG). Thioglycollate-induced sterile peritonitis was also assessed, to monitor the early events of neutrophil extravasation in wild-type and Tnfip6-deficient mice in the presence or absence of treatment with recombinant murine Tnfip6.Results. The onset of PGIA was similar, but progression and severity were significantly greater, in Tnfip6-deficient mice compared with wild-type BALB/c mice. However, this was not associated with enhanced T or B cell responses to cartilage PGs, but rather, an early and more extensive infiltration of the synovium with neutrophil leukocytes was the most prominent histopathologic feature of PGIA in Tnfip6-deficient mice. This was accompanied by elevated serum levels of interleukin-6 and amyloid A, and significantly increased activities of the enzymes plasmin, myeloperoxidase, and neutrophil elastase in the inflamed paw joints of Tnfip6-null mice, when compared with that of the wild-type littermates. Loss of control over several components of inflammation resulted in extensive and rapid cartilage degradation, bone erosion, joint ankylosis, and deformities in Tnfip6-null animals. In support of the antiinflammatory effect of Tnfip6 via the inhibition of polymorphonuclear (PMN) cell efflux, neutrophil invasion during thioglycollate-induced peritonitis was 2-fold higher in Tnfip6-deficient animals than in wild-type animals, but was dramatically suppressed by intravenous injection of recombinant murine Tnfip6.Conclusion. Tnfip6 is a multifunctional antiinflammatory protein that is produced at the site of inflammation and can be retained by the hyaluronanrich extracellular matrix. A major effect of Tnfip6 is the inhibition of the extravasation of PMN cells, predominantly neutrophils, into the site of inflammation, most likely via a CD44/hyaluronan/Tnfip6-mediated blocking mechanism.

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Isolation and characterization of eight tumor necrosis factor-induced gene sequences from human fibroblasts.

Cited by 149 publications

References 45 publications

The CXC Chemokine GCP-2/CXCL6 Is Predominantly Induced in Mesenchymal Cells by Interleukin-1β and Is Down-Regulated by Interferon-γ: Comparison with Interleukin-8/CXCL8

The CXC Chemokine GCP-2/CXCL6 Is Predominantly Induced in Mesenchymal Cells by Interleukin-1β and Is Down-Regulated by Interferon-γ: Comparison with Interleukin-8/CXCL8

Differential regulation of TSG-14 expression in murine fibroblasts and peritoneal macrophages

Enhanced neutrophil extravasation and rapid progression of proteoglycan‐induced arthritis in TSG‐6–knockout mice

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