Journal of interferon research最新文献

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Effect of interferon-gamma on membrane conformation in the macrophage-like cell line P388D. 干扰素γ对巨噬细胞样细胞系P388D膜构象的影响。
Journal of interferon research Pub Date : 1993-12-01 DOI: 10.1089/jir.1993.13.427
H Darmani, J L Harwood, S K Jackson
{"title":"Effect of interferon-gamma on membrane conformation in the macrophage-like cell line P388D.","authors":"H Darmani,&nbsp;J L Harwood,&nbsp;S K Jackson","doi":"10.1089/jir.1993.13.427","DOIUrl":"https://doi.org/10.1089/jir.1993.13.427","url":null,"abstract":"<p><p>Interferon-gamma (IFN-gamma) specifically induced the uptake of the unsaturated fatty acid [14C]linoleic acid into membrane phospholipids of the murine macrophage-like P388D cell lineage, but did not alter the incorporation of the saturated fatty acid [14C]stearic acid. Spin label ESR spectroscopy was used to examine any effects of these IFN-gamma-induced changes on membrane fluidity and the results revealed significant increases in plasma membrane fluidity. This alteration in membrane fluidity may have important consequences in the dynamic properties of cellular physiochemical interactions and some of the stimulatory effects of IFN-gamma on macrophages might be attributed to its effects on the plasma membrane composition.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 6","pages":"427-31"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.427","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19142875","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: 3
Xanthine oxidase does not mediate the antiproliferative effects of interferon-gamma in human umbilical vein endothelial cells. 黄嘌呤氧化酶不介导干扰素- γ在人脐静脉内皮细胞中的抗增殖作用。
Journal of interferon research Pub Date : 1993-12-01 DOI: 10.1089/jir.1993.13.419
L S Terada, P D Arnold
{"title":"Xanthine oxidase does not mediate the antiproliferative effects of interferon-gamma in human umbilical vein endothelial cells.","authors":"L S Terada,&nbsp;P D Arnold","doi":"10.1089/jir.1993.13.419","DOIUrl":"https://doi.org/10.1089/jir.1993.13.419","url":null,"abstract":"<p><p>Interferon-gamma (IFN-gamma) has potent antiproliferative effects on the endothelium, although the specific mechanisms responsible for this effect are not clear. We tested the hypothesis that suppression of endothelial cell proliferation by IFN-gamma is mediated by an increase in xanthine oxidase-derived O2-.. Human umbilical vein endothelial cells (HUVEC) were exposed to recombinant human IFN-gamma. We found that [3H]thymidine uptake decreased (p < 0.05) with increasing doses of IFN-gamma. Treatment of HUVEC with the xanthine oxidase inhibitor allopurinol or the O2-. scavenger superoxide dismutase had no effect (p > 0.05) on [3H]thymidine uptake of IFN-gamma-treated cells. In parallel, IFN-gamma decreased (p < 0.05) HUVEC cell counts, while allopurinol again had no effect (p > 0.05) on cell counts of IFN-gamma-treated or control HUVEC. In addition, xanthine oxidase activity of HUVEC did not (p > 0.05) increase following treatment with IFN-gamma. We conclude that IFN-gamma suppresses HUVEC proliferation by a mechanism independent of O2-. production by xanthine oxidase.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 6","pages":"419-22"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.419","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19141665","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: 4
Interferon induction by viruses. XXII. Vesicular stomatitis virus-Indiana: M-protein and leader RNA do not regulate interferon induction in chicken embryo cells. 病毒诱导干扰素。第二十二。水疱性口炎病毒-印第安纳:m蛋白和先导RNA不调节干扰素在鸡胚细胞中的诱导作用。
Journal of interferon research Pub Date : 1993-12-01 DOI: 10.1089/jir.1993.13.413
P I Marcus, M J Sekellick, C F Spiropoulou, S T Nichol
{"title":"Interferon induction by viruses. XXII. Vesicular stomatitis virus-Indiana: M-protein and leader RNA do not regulate interferon induction in chicken embryo cells.","authors":"P I Marcus,&nbsp;M J Sekellick,&nbsp;C F Spiropoulou,&nbsp;S T Nichol","doi":"10.1089/jir.1993.13.413","DOIUrl":"https://doi.org/10.1089/jir.1993.13.413","url":null,"abstract":"<p><p>Several field isolates, strains, mutants, and revertants of vesicular stomatitis virus (VSV), Indiana (IN) serotype, were studied that differed greatly in their capacity to induce interferon (IFN) in aged chick embryo cells. The predicted M-protein amino acid sequence of a wild-type field isolate that induced > or = 10,000 units/ml IFN in chicken embryo cells was identical to that of a wild-type field isolate that induced < 2 units/ml and of a noninducing wild-type laboratory strain. The 47-base plus-strand leader RNA sequences were the same for five IFN-inducing, and eight noninducing independent isolates of wild-type VSV IN. Our data show that the M-protein and plus-strand leader RNA do not of themselves regulate the induction of IFN in this system. Because the capacity of VSV IN to induce IFN resides in virion-associated elements (Marcus and Sekellick, 1987, J. Interferon Res. 7, 269-284), the differences in IFN yield observed with various isolates must result from changes in other virion components that remain to be determined.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 6","pages":"413-8"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.413","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19141664","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: 0
Expression and regulation of an interferon-alpha-inducible membrane protein p106 on human hematopoietic cells. 干扰素诱导的膜蛋白p106在人造血细胞中的表达和调控。
Journal of interferon research Pub Date : 1993-12-01 DOI: 10.1089/jir.1993.13.433
A Tolstrup, P Hokland, B Nielsen, J Justesen, M Hokland
{"title":"Expression and regulation of an interferon-alpha-inducible membrane protein p106 on human hematopoietic cells.","authors":"A Tolstrup,&nbsp;P Hokland,&nbsp;B Nielsen,&nbsp;J Justesen,&nbsp;M Hokland","doi":"10.1089/jir.1993.13.433","DOIUrl":"https://doi.org/10.1089/jir.1993.13.433","url":null,"abstract":"<p><p>p106 is a human membrane protein of 106 kD previously shown to be inducible by interferon-alpha (IFN-alpha) on Daudi cells. To investigate the role of p106 further, its distribution and inducibility within hematopoietic cells was studied. Multiparameter flow cytometry (FCM) analysis showed that p106 expression was restricted to B cells and monocytes, and in both cell lineages acquired at a late stage of differentiation. Thus, p106 was found on mature B lymphocytes and monocytes in peripheral blood and on a variety of freshly isolated leukemic cells of B and myeloid origin as well as on a variety of cultured B-cell lines. In contrast, no expression was found on T lymphocytes, natural killer (NK) cells or granulocytes. p106 expression could be further induced by IFN-alpha on monocytes and Daudi cells, and this capacity was shown to be selective for IFN-alpha, since no other cytokines tested induced p106. Moreover, IFN-alpha therapy of chronic myeloid leukemia (CML) and hairy cell leukemia (HCL) patients lead to a clearcut induction of p106 on such malignant cells. The distribution of p106 could suggest that it represents an activation antigen. Further studies, including cloning of p106 cDNA, are needed to determine the function of p106.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 6","pages":"433-41"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.433","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19142876","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
Induction of interferon in human leukocyte cultures by natural pathogenic respiratory viruses. 天然致病性呼吸道病毒诱导人白细胞培养干扰素的研究。
Journal of interferon research Pub Date : 1993-12-01 DOI: 10.1089/jir.1993.13.423
A Pitkäranta, T Hovi
{"title":"Induction of interferon in human leukocyte cultures by natural pathogenic respiratory viruses.","authors":"A Pitkäranta,&nbsp;T Hovi","doi":"10.1089/jir.1993.13.423","DOIUrl":"https://doi.org/10.1089/jir.1993.13.423","url":null,"abstract":"<p><p>Some common viruses responsible for respiratory disease have been reported to be poor inducers of interferon (IFN). Therefore, we have studied the induction of IFN in cultures of human leukocytes exposed under standardized conditions to various concentrations of adenovirus type 7A, coronavirus 229E, an influenza type A virus (H3N2), a rhinovirus, and respiratory syncytial virus (RSV). All five viruses induced substantial amounts of IFN at a multiplicity of infection of one infectious unit per cell or less. Leukocyte cultures from 50 healthy children were exposed to a standard concentration of each of the viruses. IFN was induced almost without an exception, but the amounts produced varied extensively according to both the virus and the individual leukocyte donor.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 6","pages":"423-6"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.423","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19141666","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: 17
Partial phenotypic reversion of HeLa cells by long-term interferon-alpha treatment. 长期干扰素治疗HeLa细胞的部分表型逆转。
Journal of interferon research Pub Date : 1993-10-01 DOI: 10.1089/jir.1993.13.369
O López Ocejo, S E Perea, A Reyes, L Vigoa, P López Saura
{"title":"Partial phenotypic reversion of HeLa cells by long-term interferon-alpha treatment.","authors":"O López Ocejo,&nbsp;S E Perea,&nbsp;A Reyes,&nbsp;L Vigoa,&nbsp;P López Saura","doi":"10.1089/jir.1993.13.369","DOIUrl":"https://doi.org/10.1089/jir.1993.13.369","url":null,"abstract":"<p><p>Human papillomaviruses (HPV) are associated with malignant cervical neoplasia. Several HPV-related diseases have been shown to be sensitive to interferon (IFN) treatment. HeLa cells contain and express the HPV type 18 genome and were used as a model for the evaluation of the viral expression regulation and the effect on the malignant phenotype during IFN treatment. Cells were treated continuously with 200 IU/ml IFN-alpha 2b or natural leukocyte INF-alpha for six passages (42 days). Some IFN-induced changes were observed: decrease of HPV-18 mRNA expression, changes of cell morphology, and reduction of clonogenicity in soft agar. Tumorigenicity in nude mice was not modified. Other targets of the IFN system were analyzed, and an increase of the 2',5'-oligoadenylate synthetase mRNA level and a down-regulation of type I IFN receptor were found. These results demonstrate that long-term IFN-alpha treatment induces a partial phenotypic reversion of HeLa cells to a more differentiated stage were down-regulation of HPV-18 expression could play a central role. It therefore confirms that the IFN-alpha treatment may be therapeutically useful in cervix cancer produced by HPV-18.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 5","pages":"369-75"},"PeriodicalIF":0.0,"publicationDate":"1993-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.369","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19287915","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: 4
Interference by a non-interferon-inducing subvariant of benign encephalomyocarditis virus-B with the ability of EMCV-D to produce insulin-dependent diabetes mellitus in ICR Swiss male mice. 良性脑心肌炎病毒- b的非干扰素诱导亚变体与EMCV-D在ICR瑞士雄性小鼠中产生胰岛素依赖型糖尿病的能力的干扰
Journal of interferon research Pub Date : 1993-10-01 DOI: 10.1089/jir.1993.13.363
D J Giron, S Yei
{"title":"Interference by a non-interferon-inducing subvariant of benign encephalomyocarditis virus-B with the ability of EMCV-D to produce insulin-dependent diabetes mellitus in ICR Swiss male mice.","authors":"D J Giron,&nbsp;S Yei","doi":"10.1089/jir.1993.13.363","DOIUrl":"https://doi.org/10.1089/jir.1993.13.363","url":null,"abstract":"<p><p>The D variant of encephalomyocarditis virus (EMCV-D) produces a disease syndrome that mimics insulin-dependent diabetes mellitus (IDDM) in certain mouse strains. Benign EMCV-B interferes with the ability of EMCV-D to produce IDDM. Because EMCV-B induces the production of relatively large amounts of interferon (IFN), it has been hypothesized that the interference by EMCV-B with the pathogenesis of EMCV-D is due to IFN. However, we have previously reported that in outbred ICR Swiss and inbred BALB/cByJ mice, interference by EMCV-B with the development of IDDM in response to infection with EMCV-D does not appear to involve IFN. We have isolated a subvariant of EMCV-B (EMCV-B1) which, preliminary experiments indicate, does not induce the production of detectable levels of IFN in cell culture. Studies were initiated using this subvariant to determine more conclusively if IFN is involved in interference by EMCV-B with the pathogenesis of EMCV-D. The data in the present study show that EMCV-B1 does not induce the production of detectable levels of IFN either in cell culture or in mice, but retains other reported characteristics of the parent EMCV-B, including the ability to interfere with the production of IDDM by EMCV-D in ICR Swiss male mice. These observations strengthen the hypothesis that protection of pancreatic beta cells in ICR Swiss mice by EMCV-B occurs by a mechanism other than IFN.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 5","pages":"363-8"},"PeriodicalIF":0.0,"publicationDate":"1993-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19287914","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: 6
2-Aminopurine inhibits the double-stranded RNA-dependent protein kinase both in vitro and in vivo. 2-氨基嘌呤在体外和体内均抑制双链rna依赖性蛋白激酶。
Journal of interferon research Pub Date : 1993-10-01 DOI: 10.1089/jir.1993.13.323
Y Hu, T W Conway
{"title":"2-Aminopurine inhibits the double-stranded RNA-dependent protein kinase both in vitro and in vivo.","authors":"Y Hu,&nbsp;T W Conway","doi":"10.1089/jir.1993.13.323","DOIUrl":"https://doi.org/10.1089/jir.1993.13.323","url":null,"abstract":"<p><p>The autophosphorylation of interferon (IFN)-induced double-stranded RNA-dependent p68 protein kinase (PKR) and phosphorylation of the alpha-subunit of the translation initiation factor eIF-2 were inhibited by 10 mM 2-aminopurine in vitro. High concentrations of ATP overcame the inhibition. Kinetic studies indicated that 2-aminopurine is a competitive inhibitor with respect to ATP, suggesting that these two molecules bind the same site on the kinase. Treatment of HeLa cells with poly(I):poly(C) stimulated PKR autophosphorylation in vivo. The stimulated activity was inhibited by 10 mM 2-aminopurine to approximately the same extent as the in vitro inhibition.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 5","pages":"323-8"},"PeriodicalIF":0.0,"publicationDate":"1993-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.323","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18901758","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: 121
Systemic recombinant human interferon-beta treatment of relapsing-remitting multiple sclerosis: pilot study analysis and six-year follow-up. 系统性重组人干扰素治疗复发缓解型多发性硬化:初步研究分析和6年随访。
Journal of interferon research Pub Date : 1993-10-01 DOI: 10.1089/jir.1993.13.333
R L Knobler, J I Greenstein, K P Johnson, F D Lublin, H S Panitch, K Conway, S V Grant-Gorsen, J Muldoon, S G Marcus, J C Wallenberg
{"title":"Systemic recombinant human interferon-beta treatment of relapsing-remitting multiple sclerosis: pilot study analysis and six-year follow-up.","authors":"R L Knobler,&nbsp;J I Greenstein,&nbsp;K P Johnson,&nbsp;F D Lublin,&nbsp;H S Panitch,&nbsp;K Conway,&nbsp;S V Grant-Gorsen,&nbsp;J Muldoon,&nbsp;S G Marcus,&nbsp;J C Wallenberg","doi":"10.1089/jir.1993.13.333","DOIUrl":"https://doi.org/10.1089/jir.1993.13.333","url":null,"abstract":"<p><p>A pilot study was undertaken to test the safety and establish the side effect profile of recombinant human interferon-beta 1b (Betaseron, Berlex Laboratories, Richmond, CA), in patients with relapsing-remitting multiple sclerosis (RRMS). During the initial dose finding period (24 weeks), five groups of 6 patients each were treated by subcutaneous injection three times each week with either 0.8, 4, 8, or 16 million units (mU) of Betaseron or placebo (WHO Standard). Although some side effects were noted in all groups, a dose-related trend in reduction of exacerbation frequency and side-effect profile was noted. Patients given 16 mU had no exacerbations during the initial dosing period, but associated side effects led to dose reduction or dropout. An 8 mU dose was selected for further study after 24 weeks, and continuous dosing at 8 mU in 15 patients has now exceeded 6 years. Side effects abated over time. Neutralizing antibody developed in most patients, but titers were variable, fluctuated independently of clinical course, and tended to fall with prolonged treatment. A dose-dependent rise in neopterin levels was observed during the initial dosing period. This pilot study has demonstrated responsiveness to Betaseron, shown a stable safety profile over time, and established guidelines for a dosing regimen to evaluate and optimize further the efficacy of Betaseron in RRMS.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 5","pages":"333-40"},"PeriodicalIF":0.0,"publicationDate":"1993-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19287910","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: 112
Consensus interferon induces peak mRNA accumulation at lower concentrations than interferon-alpha 2a. 共识干扰素在较低浓度下诱导mRNA的峰值积累,而不是干扰素- α 2a。
Journal of interferon research Pub Date : 1993-10-01 DOI: 10.1089/jir.1993.13.341
S B Klein, L M Blatt, M W Taylor
{"title":"Consensus interferon induces peak mRNA accumulation at lower concentrations than interferon-alpha 2a.","authors":"S B Klein,&nbsp;L M Blatt,&nbsp;M W Taylor","doi":"10.1089/jir.1993.13.341","DOIUrl":"https://doi.org/10.1089/jir.1993.13.341","url":null,"abstract":"<p><p>The biological activity of a novel recombinant interferon, r-metIFN-con1, which represents a consensus sequence of the most commonly appearing amino acids at each locus of 14 naturally occurring IFN-alpha s, was assessed and compared to that of IFN-alpha 2a. The increase in cellular mRNA levels for three IFN-inducible genes served as a quantitative measure of the effectiveness of the stimulation by each of the IFNs. Three cell lines were treated with equimolar amounts of two IFNs encompassing a 5 log range and mRNA was extracted at five different times after treatment. In all cases, r-metIFN-con1 produced mRNA increases at lower concentrations than IFN-alpha 2a. HLA-DR alpha mRNA, which is not affected by IFN-alpha in ME180 or Daudi cells, was also not affected by r-metIFN-con1. However, in Eskol cells, both IFNs effected an increase in HLA-DR alpha mRNA to similar levels. The r-metIFN-con1 was effective at approximately 10-fold lower molar concentrations. At effective concentrations (10-fold lower molar dose of r-metIFN-con1), both IFNs produced similar kinetics of accumulation of all three mRNAs tested. r-metIFN-con1 is therefore more effective than IFN-alpha 2a at the level of mRNA regulation as well as the antiviral and antiproliferative activities that have been reported previously.</p>","PeriodicalId":16268,"journal":{"name":"Journal of interferon research","volume":"13 5","pages":"341-7"},"PeriodicalIF":0.0,"publicationDate":"1993-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/jir.1993.13.341","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19287911","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: 18
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