Type I Interferon
Mostrando 13-24 de 450 artigos, teses e dissertações.
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13. ACTIVITY OF SWINE TYPE I INTERFERON IN PROTECTION AGAINST FOOT-AND-MOUTH DISEASE VIRUS (FMDV) / ATIVIDADE DO INTERFERON TIPO I SUÍNO NA PROTEÇÃO CONTRA O VÍRUS DA FEBRE AFTOSA (FMDV)
The objective of this study is to evaluate the adjuvant effect of interferon alpha (IFNα) in swine vaccinated with a recombinant replication-defective adenovirus containing foot-and-mouth disease virus (FMDV) protein coding regions, as well as to understand the molecular mechanisms involved in the interaction of FMDV with its host. In the first part of
Publicado em: 2005
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14. Clinical and immunological consequences of human T cell leukemia virus type-I and Schistosoma mansoni co-infection
Human T cell leukemia virus type-I (HTLV-I) infection is associated with spontaneous T cell activation and uncontrolled lymphocyte proliferation. An exacerbated type-1 immune response with production of pro-inflammatory cytokines (interferon-gamma and tumor necrosis factor-alpha) is significantly higher in patients with myelopathy associated to HTLV-I than i
Memórias do Instituto Oswaldo Cruz. Publicado em: 2004-08
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15. Cytokine profile associated with human chronic schistosomiasis mansoni
This study objective was to evaluate the cytokines associated with early events of hepatic fibrosis in schistosomiasis mansoni. Hepatic fibrosis was classified by ultrasonography in 94 patients. Immunological evaluation was performed by measurement of secreted cytokines (interleukin IL-5, IL-10, IL-13, interferon-gamma, tumor necrosis factor-alpha and transf
Memórias do Instituto Oswaldo Cruz. Publicado em: 2004-08
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16. Leishmania (Leishmania) major-infected rhesus macaques (Macaca mulatta) develop varying levels of resistance against homologous re-infections
Seven rhesus macaques were infected intradermally with 10(7) promastigotes of Leishmania (Leishmania) major. All monkeys developed a localized, ulcerative, self-healing nodular skin lesion at the site of inoculation of the parasite. Non-specific chronic inflammation and/or tuberculoid-type granulomatous reaction were the main histopathological manifestations
Memórias do Instituto Oswaldo Cruz. Publicado em: 2001-08
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17. Differential efficacies of human type I and type II interferons as antiviral and antiproliferative agents.
Treatment of human fibroblast FS-4 cultures with human type II interferon preparations induced the synthesis of at least four proteins that were similar in size to four of the five proteins induced by type I interferons (Mr 120,000, 88,000, 67,000, and 56,000). However, the Mr 67,000 and 56,000 proteins were induced more strongly by type II than by type I in
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18. Mouse fibroblast (type I) and immune (type II) interferons: pronounced differences in affinity for gangliosides and in antiviral and antigrowth effects on mouse leukemia L-1210R cells.
Different interferons can be obtained from the same animal species depending on the cells and (or) the inducers used. Interferons of type I and type II differ not only antigenically but also in molecular weight and stability at low pH. We have investigated whether mouse type I and type II interferons also differ in properties relating to their biological act
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19. Mice devoid of interferon regulatory factor 1 (IRF-1) show normal expression of type I interferon genes.
The transcription factor interferon regulatory factor 1 (IRF-1) binds tightly to the interferon (IFN)-beta promoter and has been implicated in the induction of type I IFNs. We generated mice devoid of functional IRF-1 by targeted gene disruption. As reported by others, IRF-1-deficient mice showed a discrete phenotype: the CD4/CD8 ratio was increased and IFN-
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20. Dissection of the interferon gamma-MHC class II signal transduction pathway reveals that type I and type II interferon systems share common signalling component(s).
We have used a herpes virus thymidine kinase (HSV-TK) based metabolic selection system to isolate mutants defective in the interferon gamma mediated induction of the MHC class II promoter. All the mutations act in trans and result in no detectable induction of MHC and invariant chain (Ii) gene expression. Scatchard analysis indicates that the mutants have a
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21. Cellular source of interferons in the circulation of mice with delayed hypersensitivity.
The cellular origins of type I and type II interferons released into the circulation of mice with delayed hypersensitivity were investigated. We determined the effect of treatment with various immunosuppressive agents, including cyclophosphamide, cycloheximide, antithymocyte serum, and whole-body X-irradiation, on the release of interferons after intravenous
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22. Type I and II interferons and migration inhibitory factor: production in Mycobacterium bovis BCG-infected mice desensitized with old tuberculin or lipopolysaccharide.
Mice with delayed hypersensitivity induced by infection with Mycobacterium bovis strain BCG were desensitized by a single large dose of specific antigen (old tuberculin, OT) or a nonspecific interferon stimulus (bacterial lipopolysaccharide, LPS). Subsequent challenge of the desensitized animals revealed only a homologous hyporeactivity, that is, mice desens
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23. Interferon Synthesis in X-Irradiated Animals V. Origin of Mouse Serum Interferon Induced by Polyinosinic-Polycytidylic Acid and Encephalomyocarditis Virus
The radioresistant cell systems producing serum interferon after intravenous administration of polyinosinic-polycytidylic acid [poly(I·C)] or encephalomyocarditis virus in mice were studied in rat-to-mouse radiation chimeras. Interferon induced by poly(I·C) became of donor type within 3 months after grafting of irradiated C3H/He mice with Wistar rat bone m
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24. A Kaposi's sarcoma-associated herpesviral protein inhibits virus-mediated induction of type I interferon by blocking IRF-7 phosphorylation and nuclear accumulation
Interferons constitute the earliest immune response against viral infection. They elicit antiviral effects as well as multiple biological responses involved in cell growth regulation and immune activation. Because the interferon-induced cellular antiviral response is the primary defense mechanism against viral infection, many viruses have evolved strategies
National Academy of Sciences.