F A Montero-Julian, E Gautherot, J Wijdenes, B Klein, H Brailly
{"title":"Pharmacokinetics of interleukin-6 during therapy with anti-interleukin-6 monoclonal antibodies: enhanced clearance of interleukin-6 by a combination of three anti-interleukin-6 antibodies.","authors":"F A Montero-Julian, E Gautherot, J Wijdenes, B Klein, H Brailly","doi":"10.1089/jir.1994.14.301","DOIUrl":"https://doi.org/10.1089/jir.1994.14.301","url":null,"abstract":"","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"301-2"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.301","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18859756","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}
Patients with chronic hepatitis C were treated with interferon (IFN) and followed for hepatitis C virus (HCV) RNA and antibody to HCV (anti-HCV) in serum. The response was correlated with decrease in serum levels of HCV RNA, as well as HCV genotypes and liver histopathology. Response to IFN, estimated by clearance of HCV RNA and normalization of aminotransferase levels at 6 months after the withdrawal of IFN, was observed in 11 (31%) of 35 patients infected with HCV of genotype II/1b, 13 (72%) of 18 with genotype III/2a, and 2 (33%) of 6 with genotype IV/2b; a single patient with genotype I/1a responded while the one doubly infected with HCV of genotypes II/1b and IV/2b did not. Response was seen in 10 (71%) of 14 patients with chronic persistent hepatitis, 14 (39%) of 36 with chronic active hepatitis 2A, and 3 (27%) of 11 with 2B. Response was achieved less often in patients with high than low pretreatment levels of HCV RNA. HCV RNA dropped sharply on a day after the start of IFN, and continued to decrease during the 2 weeks, irrespective of the response to IFN or HCV genotypes. In contrast, anti-HCV decreased more gradually and only in responders to IFN. These results support the rapid development of an IFN-mediated antiviral effect on HCV, and support therapeutic effects of IFN dependent on histopathology of liver as well as HCV RNA titers and genotypes.
{"title":"Prompt decrease of circulating hepatitis C virus in patients with chronic hepatitis C after treatment with interferon.","authors":"H Saitoh, S Naitoh, H Okamoto, Y Akahane","doi":"10.1089/jir.1994.14.239","DOIUrl":"https://doi.org/10.1089/jir.1994.14.239","url":null,"abstract":"Patients with chronic hepatitis C were treated with interferon (IFN) and followed for hepatitis C virus (HCV) RNA and antibody to HCV (anti-HCV) in serum. The response was correlated with decrease in serum levels of HCV RNA, as well as HCV genotypes and liver histopathology. Response to IFN, estimated by clearance of HCV RNA and normalization of aminotransferase levels at 6 months after the withdrawal of IFN, was observed in 11 (31%) of 35 patients infected with HCV of genotype II/1b, 13 (72%) of 18 with genotype III/2a, and 2 (33%) of 6 with genotype IV/2b; a single patient with genotype I/1a responded while the one doubly infected with HCV of genotypes II/1b and IV/2b did not. Response was seen in 10 (71%) of 14 patients with chronic persistent hepatitis, 14 (39%) of 36 with chronic active hepatitis 2A, and 3 (27%) of 11 with 2B. Response was achieved less often in patients with high than low pretreatment levels of HCV RNA. HCV RNA dropped sharply on a day after the start of IFN, and continued to decrease during the 2 weeks, irrespective of the response to IFN or HCV genotypes. In contrast, anti-HCV decreased more gradually and only in responders to IFN. These results support the rapid development of an IFN-mediated antiviral effect on HCV, and support therapeutic effects of IFN dependent on histopathology of liver as well as HCV RNA titers and genotypes.","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"239-44"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.239","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18540601","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}
S Kadereit, J Galabru, N Robert, E F Meurs, A G Hovanessian
Polyclonal antibodies raised against purified and urea-denatured double-stranded protein kinase (PKR) from human origin cross-reacted by immunoblotting with a 48-kD protein (p48) induced by the three types of interferon (IFN), alpha, beta, and gamma. The induction of p48 is IFN dose dependent and its accumulation occurs a few hours after the addition of IFN. The induction of p48 is blocked by actinomycin D. Analysis by two-dimensional gel isoelectric-focusing, revealed p48 as a single spot with an isoelectric point (pI) of 6.8. In the same experiment the PKR was revealed as several subspecies with pI values in the pH range of 7.4-8.0. Cell fractionation experiments indicated that PKR and p48 have different subcellular localizations: PKR was found to be associated with the microsomal pellet as shown previously whereas p48 was recovered in the microsomal supernatant fraction. In addition to these differences, PKR and p48 were found to be differentially expressed in some human cells treated with the three types of IFN. For example, in HeLa cells, IFN-alpha or IFN-beta induced similarly both PKR and p48 whereas IFN-gamma induced mainly p48. In U937 cells in which PKR was not expressed with or without IFN treatment, p48 was strongly induced by all three types of IFN. These results suggest different mechanisms for the induction of PKR and p48. In view of its presence in different types of human cells and its induction by different types of IFN, it is possible to suggest that p48 might play an important role in mediating some of the action of IFN.
{"title":"Characterization of an interferon-induced 48-kD protein immunologically related to the double-stranded RNA-activated protein kinase PKR.","authors":"S Kadereit, J Galabru, N Robert, E F Meurs, A G Hovanessian","doi":"10.1089/jir.1994.14.251","DOIUrl":"https://doi.org/10.1089/jir.1994.14.251","url":null,"abstract":"<p><p>Polyclonal antibodies raised against purified and urea-denatured double-stranded protein kinase (PKR) from human origin cross-reacted by immunoblotting with a 48-kD protein (p48) induced by the three types of interferon (IFN), alpha, beta, and gamma. The induction of p48 is IFN dose dependent and its accumulation occurs a few hours after the addition of IFN. The induction of p48 is blocked by actinomycin D. Analysis by two-dimensional gel isoelectric-focusing, revealed p48 as a single spot with an isoelectric point (pI) of 6.8. In the same experiment the PKR was revealed as several subspecies with pI values in the pH range of 7.4-8.0. Cell fractionation experiments indicated that PKR and p48 have different subcellular localizations: PKR was found to be associated with the microsomal pellet as shown previously whereas p48 was recovered in the microsomal supernatant fraction. In addition to these differences, PKR and p48 were found to be differentially expressed in some human cells treated with the three types of IFN. For example, in HeLa cells, IFN-alpha or IFN-beta induced similarly both PKR and p48 whereas IFN-gamma induced mainly p48. In U937 cells in which PKR was not expressed with or without IFN treatment, p48 was strongly induced by all three types of IFN. These results suggest different mechanisms for the induction of PKR and p48. In view of its presence in different types of human cells and its induction by different types of IFN, it is possible to suggest that p48 might play an important role in mediating some of the action of IFN.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"251-7"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18540602","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}
{"title":"Use of anti-tumor necrosis factor antibodies in rheumatoid arthritis.","authors":"M Feldmann, M J Elliott, F M Brennan, R N Maini","doi":"10.1089/jir.1994.14.299","DOIUrl":"https://doi.org/10.1089/jir.1994.14.299","url":null,"abstract":"","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"299-300"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.299","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18859755","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}
I Schedel, M Ballmaier, F Rohde, U Süttmann, H Deicher
{"title":"Ketotifen inhibits tumor necrosis factor alpha production in the peripheral blood mononuclear cells of patients infected with human immunodeficiency virus.","authors":"I Schedel, M Ballmaier, F Rohde, U Süttmann, H Deicher","doi":"10.1089/jir.1994.14.291","DOIUrl":"https://doi.org/10.1089/jir.1994.14.291","url":null,"abstract":"","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"291-2"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.291","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18859752","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}
R Kamijo, D Shapiro, J Gerecitano, J Le, M Bosland, J Vilcek
{"title":"Mycobacterium bovis infection of mice lacking receptors for interferon-gamma or for transcription factor IRF-1.","authors":"R Kamijo, D Shapiro, J Gerecitano, J Le, M Bosland, J Vilcek","doi":"10.1089/jir.1994.14.281","DOIUrl":"10.1089/jir.1994.14.281","url":null,"abstract":"","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"281-2"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.281","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18859748","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}
{"title":"Interleukin-1 antagonists.","authors":"C A Dinarello","doi":"10.1089/jir.1994.14.307","DOIUrl":"https://doi.org/10.1089/jir.1994.14.307","url":null,"abstract":"","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"307"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.307","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18859759","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}
{"title":"Interleukin-4 and interleukin-10 as antagonists of interferon-gamma.","authors":"P Miossec","doi":"10.1089/jir.1994.14.285","DOIUrl":"https://doi.org/10.1089/jir.1994.14.285","url":null,"abstract":"","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"14 5","pages":"285"},"PeriodicalIF":0.0,"publicationDate":"1994-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1994.14.285","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18540605","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}
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