B cell growth modulating and differentiating activity of recombinant human 26-kd protein (BSF-2, HuIFN-beta 2, HPGF).

Poupart, P.; Vandenabeele, Peter; Cayphas, Sylvie; Snick, Jacques Van; Haegeman, Guy; Kruys, Véronique; Fiers, Walter; Content, Jean

doi:10.1002/j.1460-2075.1987.tb02357.x

Cited by 206 publications

(66 citation statements)

References 27 publications

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“…Each of the IFN species tested increased the surface expression of class I antigens maximally after 24 to 48 hours (data not shown), lnterieukin-6 (IL-6), (also known as /Mnterferon, B cell stimulatory factor 2, or hepatic stimulatory factor) 27 had no significant effect on the surface expression of class I antigens on SMC (Figure 3). …”

Section: Class I Hla Expressionmentioning

confidence: 95%

Regulation of major histocompatibility gene expression in human vascular smooth muscle cells.

1989

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Section: Class I Hla Expressionmentioning

confidence: 95%

Regulation of major histocompatibility gene expression in human vascular smooth muscle cells.

1989

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“…Several pleiotropic effects of IL-1/3 are mediated by IL-6, a cytokine previously identified as a B cellstimulating factor (Poupart et al, 1987). These cytokines are strongly synergistic in various immunological processes, including induction of cell proliferation and acute-phase protein synthesis by hepatocytes (Tritarelli et al, 1994;Conti et al, 1995), and IL-i/3 is an important stimulator of IL-6 production in peripheral organs (Akira et al, 1990).…”

Section: Cox-1 Isoformmentioning

confidence: 99%

Effect of Acute Systemic Inflammatory Response and Cytokines on the Transcription of the Genes Encoding Cyclooxygenase Enzymes (COX‐1 and COX‐2) in the Rat Brain

Lacroix

Rivest

1998

Journal of Neurochemistry

251

136

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Abstract:The aim of this study was to investigate the influence of the acute-phase response and the promflammatory cytokines on the transcription of the genes encoding the limiting enzymes for the production of prostaglandins, cyclooxygenase (COX)-1 and COX-2, in the rat brain. The bacterial endotoxin lipopolysaccharide (intravenous and intraperitoneal) and turpentine (intramuscular) were used as different models of inflammation in adult male rats. Animals were also killed at various times after intravenous administration of interleukin-1/3, tumor necrosis factor-a, and interleukin-6, and mRNAs encoding COX-1 and COX-2 were assayed by in situ hybridization histochemistry. A profound transcriptional activation of the gene encoding COX-2 was detected over blood vessels of the entire brain microvasculature, choroid plexus, and leptomeninges of lipopolysaccharide-challenged rats. Injection of the endotoxin intravenously also increased COX-2 gene expression within parvocellular division of the hypothalamic paraventricular nucleus. It is interesting that intramuscular turpentine injection stimulated transcription of COX-2 along endothelium of brain capillaries, and the signal of this transcript paralleled the inflammation of the left hind limb. A robust COX-2 mRNA signal was detected rapidly in the brain microvessels of interleukin-1~3-injectedrats, whereas tumor necrosis factor-a administration caused a modest but significant induction of this transcript. In contrast, intravenous injection of interleukin-6 did not alter genetic expression of COX-2, and none of the above described models affected the synthesis of COX-1 gene in the rat brain. These results indicate that specific cell populations, in particular vascular-and/or perivascular-associated cells, are responsible for the central production of prostaglandins during systemic inflammation, and circulating interleukin-1~is likely to be a potent mediator of this response. Key Words: In situ hybridization histochemistry-Immune responseInterleukin -1 -Interleukin -6-Leptomeninges -Lipopolysaccharide-Microvessels--Paraventricular nucleus of the hypothalamus-Prostaglandins-Tumor necrosis factor-Turpentine insult.

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“…On the basis of their molecular structures, it was recognized recently that interferon-p2 [l], B-cell stimulatory factor-2 [2], 26-kDa protein [3], hybridoma plasmacytoma growth factor [4] and hepatocyte-stimulating factor [5, 61, although having been isolated from several cell types, are identical molecules [4-81. To overcome the confusion in nomenclature, it was suggested this molecule be named interleukin-6 (IL-6) [8].…”

mentioning

confidence: 99%

Fate of interleukin‐6 in the rat

Castell

Klapproth

Groß

et al. 1990

European Journal of Biochemistry

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Iodinated recombinant human interleukin‐6(125I‐rhIL‐6) was intravenously injected into rats and its fate was studied during 24 h. Between 10–20 min after a single‐dose injection, 125I‐rhIL‐6 accumulated in liver as previously reported [Castell et al. (1988) Eur. J. Biochem. 177, 357–361]. After 1 h. the radioactivity disappeared from the liver and accumulated in skin, reaching 35% of injected 125I‐rhIL‐6 5–8 h after injection. No comparable accumulation of radioactivity was found in skin when [125I]iodide or rat serum 125I‐albumin was administered. Finally the radioactivity was detected as [125I]iodide in urine. Autoradiograhic analysis of skin sections 5 h after 125‐I‐rhIL‐6 injection showed radioactivity in the interstitium. When the experiments were carried out with [35S]rhIL‐6, essentially the same results were obtained: a decrease in radioactivity in the liver after 20 min, and a substantial increase in skin 7 h after injection. In vitro experiments showed that 125I‐rhIL‐6 is degraded by rat and human fibroblasts, whereas no degradation was observed with rat hepatoma cells (Fao) or human hepatocytes. These observations suggest the involvement of skin in the catabolism of IL‐6.

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B cell growth modulating and differentiating activity of recombinant human 26-kd protein (BSF-2, HuIFN-beta 2, HPGF).

Abstract: The human '26-kd protein' is a secreted glycoprotein expressed, for example, in (blood) Here we show that the recombinant 26-kd protein exhibits a high growth factor activity when assayed on an IL-

Cited by 206 publications

References 27 publications

Regulation of major histocompatibility gene expression in human vascular smooth muscle cells.

Regulation of major histocompatibility gene expression in human vascular smooth muscle cells.

Effect of Acute Systemic Inflammatory Response and Cytokines on the Transcription of the Genes Encoding Cyclooxygenase Enzymes (COX‐1 and COX‐2) in the Rat Brain

Fate of interleukin‐6 in the rat

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