Journal of interferon research最新文献_第2页

Modulation of interferon-mediated inhibition of human immunodeficiency virus type 1 by Tat. 干扰素介导的Tat对人类免疫缺陷病毒1型抑制的调节

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.259

Y Shirazi, W Popik, P M Pitha

引用次数: 10

Soluble interferon-gamma receptor: a therapeutically useful drug for systemic lupus erythematosus. 可溶性干扰素-γ 受体：治疗系统性红斑狼疮的有效药物。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.283

L Ozmen, D Roman, M Fountoulakis, G Schmid, B Ryffel, G Garotta

引用次数: 6

Selective interferon-alpha/beta effects on platelet-derived growth factor-stimulated processes in quiescent BALB/c-3T3 fibroblasts. 选择性干扰素- α / β对静止BALB/c-3T3成纤维细胞血小板衍生生长因子刺激过程的影响

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.265

I Tamm, T Kikuchi, D Kreutter, W J Pledger, L M Pfeffer

引用次数: 5

Interferon expression in Crohn's disease patients: increased interferon-gamma and -alpha mRNA in the intestinal lamina propria mononuclear cells. 克罗恩病患者干扰素表达:肠固有层单核细胞中干扰素γ和α mRNA升高。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.235

S Fais, M R Capobianchi, M Silvestri, F Mercuri, F Pallone, F Dianzani

{"title":"Interferon expression in Crohn's disease patients: increased interferon-gamma and -alpha mRNA in the intestinal lamina propria mononuclear cells.","authors":"S Fais, M R Capobianchi, M Silvestri, F Mercuri, F Pallone, F Dianzani","doi":"10.1089/jir.1994.14.235","DOIUrl":"https://doi.org/10.1089/jir.1994.14.235","url":null,"abstract":"The in vivo interferon (IFN) activation in Crohn's disease was evaluated by measuring the relative amounts of IFN-alpha and -gamma mRNA in freshly isolated human lamina propria mononuclear cells (LPMC) from patients with Crohn's disease and controls. Both IFN-gamma and IFN-alpha mRNA, as estimated by dot blot analysis, were increased in Crohn's disease (LPMC), although the relative amounts of IFN mRNA appeared to differ among patients. Appreciable amounts of IFN-gamma mRNA were found in Crohn's disease peripheral blood mononuclear cells (PBMC) extracts, whereas the same cells were negative for IFN-alpha mRNA. Only minute amounts of IFN-gamma RNA were found sporadically in control LPMC while no IFN-alpha was detected. Control PBMC were shown to be virtually negative for both IFN-alpha and IFN-gamma mRNA. These data suggest that IFN induction in the normal human gut is a well-controlled function and that in Crohn's disease tissues, both IFN-gamma and IFN-alpha production are dysregulated. The increased IFN activity may represent a major feature in the induction and perpetuation of the chronic inflammatory process in Crohn's disease.","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"235-8"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18861951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 57

Effects of anti-interferon-gamma and anti-interleukin-6 antibodies in disease models in mice: antibodies as carriers of cytokines. 抗干扰素- γ和抗白细胞介素-6抗体在小鼠疾病模型中的作用:抗体作为细胞因子的载体。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.277

A Billiau, P Matthys, E Martens, H Heremans

引用次数: 7

Induction in interferon-alpha/beta-treated hepatocytes of the inhibitor of the multiplication of IFN-alpha/beta-resistant Friend leukemia cells. 干扰素- α / β处理的肝细胞中ifn - α / β抗性Friend白血病细胞增殖抑制剂的诱导。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.245

H Yasui, O Takikawa, T Oku, R Yoshida

{"title":"Induction in interferon-alpha/beta-treated hepatocytes of the inhibitor of the multiplication of IFN-alpha/beta-resistant Friend leukemia cells.","authors":"H Yasui, O Takikawa, T Oku, R Yoshida","doi":"10.1089/jir.1994.14.245","DOIUrl":"https://doi.org/10.1089/jir.1994.14.245","url":null,"abstract":"We reported previously that interferon-alpha/beta (IFN-alpha/beta)-treated hepatocytes in culture released a soluble factor(s) that suppressed the multiplication of an INF-alpha/beta-resistant clone of Friend leukemia cells (FLCs). To characterize the factor(s) further, we first examined the possibility that products of nonparenchymal cells (NPCs) included in small number in the hepatocyte cultures were involved in the inhibitory activity. We prepared cultures of purified adherent NPCs, mostly Kupffer cells, and sinusoidal endothelial cells, and culture supernatants of NPCs pretreated with IFN-alpha/beta were tested for the inhibitory activity for FLC multiplication. IFN did not induce any inhibitory activity in NPC cultures, whereas LPS-stimulated NPCs cultivated in parallel released several inhibitory factors including tumor necrosis factor-alpha (TNF-alpha). To explore the possibility that IFN augmented the release of hepatocyte cytosolic proteins, including arginase, we compared the inhibitory activity in culture supernatant of IFN-treated hepatocytes with that found in hepatocyte extract by anion-exchange chromatography. The IFN-induced inhibitory activity was eluted at relatively high salt concentration as a single peak, while the inhibitory activity in hepatocyte extract was co-eluted with arginase at low salt concentration. These results suggested that IFN induced production by hepatocytes of an inhibitor of FLC multiplication.","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"245-50"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.245","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18859746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Interferon-alpha as an antagonist to proinflammatory and hematopoietic cytokines. 干扰素- α作为促炎和造血细胞因子的拮抗剂。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.289

C Peschel, M J Aman, C Huber

引用次数: 1

Interleukin-6 antibodies in rheumatoid arthritis. 类风湿关节炎中的白细胞介素-6抗体。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.297

J Wijdenes, E Racadot, D Wendling

引用次数: 11

Interleukin-1 receptor antagonist and genetic susceptibility to inflammation. 白细胞介素-1受体拮抗剂与炎症的遗传易感性。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.305

G W Duff

引用次数: 6

The type I interferon system is locally activated in psoriatic lesions. I型干扰素系统在银屑病病变中被局部激活。

Journal of interferon research Pub Date : 1994-10-01 DOI: 10.1089/jir.1994.14.229

P Schmid, P Itin, D Cox, G K McMaster, M A Horisberger

{"title":"The type I interferon system is locally activated in psoriatic lesions.","authors":"P Schmid, P Itin, D Cox, G K McMaster, M A Horisberger","doi":"10.1089/jir.1994.14.229","DOIUrl":"https://doi.org/10.1089/jir.1994.14.229","url":null,"abstract":"The expression of mRNAs encoding interferons (IFNs) and IFN-inducible proteins has been studied in psoriatic lesions and in noninvolved skin. The specific mRNAs have been detected by in situ hybridization using antisense RNAs. Signals for the expression of IFN-gamma mRNA have been found exclusively in cells of psoriatic lesions, and most likely represent a subpopulation of infiltrating leukocytes. Weak signals of IFN-alpha mRNA have been detected throughout the hyperkeratotic epidermis, although specific signals for IFN-beta mRNA expression were not detectable. The expression of two IFN-alpha-inducible gene products, namely the MxA protein and the 2'-5' oligoadenylate (2-5A) synthetase, have been studied as markers for the local activation of the IFN-alpha system. Expression of MxA mRNA and protein was observed in psoriatic keratinocytes, but not in normal appearing keratinocytes adjacent to the lesions. Similarly, 2-5A synthetase expression was markedly elevated in psoriatic keratinocytes. The results of the present study indicate that the IFN-alpha system is selectively activated in psoriatic lesions, although it remains silent in noninvolved skin. The implications of this finding are discussed within the boundaries of current understanding of the cytokine network.","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"229-34"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18861950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 55