2 edition of Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells found in the catalog.
Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells
Paul Thomas Tomkins
Thesis (Ph.D.) - University of Warwick, 1989.
|Statement||by Paul Thomas Tomkins.|
A semicontinuous infection system was used to test viral replication and interferon induction in lymphoblastoid cells: measles virus, Newcastle disease virus (NDV), Sendai virus, human parainfluenza virus (type II and III), Semliki forest virus (SFV) and Vesicular stomatitis virus (VSV). With the exception of Sendai virus, all viruses replicated in the Namalva cell line. Semliki Forest virus (SFV) infection of mice is a useful model of viral neuropathogenesis in animals and avirulent strains such as SFV-A7 induce immune-mediated demyelination and death of neurones.
Persistence of Virulent Semliki Forest Virus in Mouse Brain Following Co-inoculation with Defective Interfering Particles Article (PDF Available) in Journal of General Virology 67 (Pt 6)(6) We have previously reported that the absence of sphingosine kinase 1 (SK1) affects both dengue virus (DENV) infection and innate immune responses in vitro. Here we aimed to define SK1-dependancy of DENV-induced disease and the associated innate responses in vivo. The lack of a reliable mouse model with a fully competent interferon response for DENV infection is a challenge, .
Cytokines are important mediators in the pathogenesis of central nervous system (CNS) inflammatory diseases including multiple sclerosis (MS), experim. We have previously reported that the absence of sphingosine kinase 1 (SK1) affects both dengue virus (DENV) infection and innate immune responses in we aimed to define SK1-dependancy of DENV-induced disease and the associated innate responses in lack of a reliable mouse model with a fully competent interferon response for DENV infection is a challenge, and here we use an.
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Morris A, Tomkins PT, Maudsley DJ, Blackman M. Infection of cultured murine brain cells by Semliki Forest virus: effects of interferon-alpha beta on viral replication, viral antigen display, major histocompatibility complex antigen display and lysis by cytotoxic T lymphocytes.
J Gen Virol. Jan; 68 (Pt 1)–Cited by: 9. Tomkins, Paul Thomas () Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells. PhD thesis, University of Warwick.
PreviewAuthor: Paul Thomas Tomkins. Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells G cells, prior to treatment with a β-propiolactone inactivated preparation of SFV, increased the ability of the cells to stimulate SFV-specific T-cell release of IFN-γ.
This increased ability correlated with an increase in MHC antigen Author: Paul Thomas Tomkins. Interferon modulation of T-cell responses to Semliki Forest virus infected murine brain cells. Thesis (Thesis) Find all citations by this author (default).Author: Paul Thomas Tomkins. The viral genotype may influence the response to interferon (IFN) treatment in chronic hepatitis C virus (HCV) infection.
To characterize potential mechanisms responsible for this effect, we assessed whether IFN modulation of HCV‐specific T‐cell responses differs in patients infected by different by: Gamma interferon production and cytotoxicity of spleen cells from mice infected with Semliki Forest Virus.
J Gen Virol Discussion HC Thomas (London, U.K.): Dr Morris men- tioned that in the context of the liver he knew of no data to show that there is modulation of HLA class I proteins during infection. TABLE 1. Percentages of brain-infiltrating T cells expressing the indicated cytokines at day 70 postinfection - "T Cells Facilitate Recovery from Venezuelan Equine Encephalitis Virus-Induced Encephalomyelitis in the Absence of Antibody".
Type I IFN reduces cholesterol synthesis upon CMV, herpes simplex (HSV1), semliki forest virus, vaccinia virus (VV), and adenovirus (ADV) infection in bone marrow-derived macrophages, which is dependent on IFNAR1 and TYK2.
Similarly, infection with murine gammaherpesvirus (MHV) reduces cholesterol and long chain FAS in macrophages. FIGURE 1. IFN-a and -~ each blocks the Ia-inducing activity of IFN-% [email protected] were obtained from C3H/He .4) or (B, C) mice that had been injected with thioglycollate medium 4 d previously.
After washing off nonadherent cells and preventing cell growth with mitomycin C, we added IFN--r ( IU/ml) simultaneously with (A) 1FN-et/,8, (B) IFN-a, or (C) IFN-/3 at the indicated doses. The. Type I interferons (IFN) are well studied cytokines with anti-viral and immune-modulating functions.
Type I IFNs are produced following viral infections, but until recently, the mechanisms of. Park HJ, Park JS, Jeong YH, Son J, Ban YH, Lee BH, et al. PD-1 upregulated on regulatory T cells during chronic virus infection enhances the suppression of CD8+ T cell immune response via the interaction with PD-L1 expressed on CD8+ T cells.
Journal of immunology. ;(12)– pmid View Article. Epithelial cells secrete interferon-b as an initial response to viral infection (Marie et al., ).
Dendritic cells are able to produce INFa subtypes (Diebold et al., ).However, the. INTRODUCTION TO THE INTERFERON SYSTEM. Interferon (IFN) was discovered as an antiviral agent during studies on virus interference (, ).Isaacs and Lindenmann reported in that influenza virus-infected chick cells produced a secreted factor that mediated the transfer of a virus-resistant state active against both homologous and heterologous viruses ().
Interferon-gamma (IFN-γ) is a pleiotropic cytokine produced by T cells and NK cells that has been implicated as a deleterious factor in MS, the immune-mediated demyelinating disorder. In vitro, purified developing and mature oligodendrocytes die in the presence of IFN-γ by apoptosis and necrosis, respectively.
Immune system - Immune system - Interferons: Another group of proteins that provide protection are the interferons, which inhibit the replication of many—but not all—viruses.
Cells that have been infected with a virus produce interferon, which sends a signal to other cells of the body to resist viral growth. When first discovered ininterferon was thought to be a single substance.
In vivo, a strong upregulation of TLR-3 expression occurred in the brain of mice infected by Semliki forest virus (SFV). This upregulation of TLR-3 was itself dependent on the type I IFN response, in a positive feed-back loop. TLR-7, -8, -9 receptors sense pathogens motifs, such.
Mice adoptively‐sensitized to develop chronic relapsing experimental autoimmune encephalomyelitis (EAE), a model for the human demyelinating condition, multiple sclerosis (MS), were given injections of recombinant human IL‐10 at various timepoints post‐sensitization in an attempt to.
Tomkins PT, Ward GA, Morris AG. Role of interferon-gamma in T-cell responses to Semliki Forest virus-infected murine brain cells. Immunology. Mar; 63 (3)– [PMC free article] Atkins GJ, Johnston MD, Westmacott LM, Burke DC.
Department of Biological Sciences, University of Warwick, Coventry, CV47AL, England. J Gen Virol. Virus infection was readily observed in the myocardium, endocardium, exocrine pancreas, adipose tissue, smooth muscle cells and in the brain in meningeal cells, ependymal cells and oligodendrocytes.
Abstract We report a review of all the experimental and clinical studies performed in the last 60 years on the antiviral activity of inactivated Corynebacterium parvum (Cutibacterium acnes).
This b. Semliki Forest virus (SFV) infection of mice provides a useful model for the analysis of viral neuropathogenesis. In this study, the roles of interferon (IFN)-gamma and nitric oxide (NO) in the. NK cells are known not only to be a key player in regulating anti-viral response but also for having a response against some cancers, like acute myeloid leukemia, 67 Because NK cells play a key role in anti-viral response, cytokine control of NK cells using a virus can allow us to regulate the level of immune response in order to balance.Type I interferons (IFN-Is) are emerging as key drivers of inflammation and immunosuppression in chronic infection.
Control of these infections requires IFN-I signaling; however, prolonged IFN-I signaling can lead to immune dysfunction. IFN-Is are also emerging as double-edged swords in cancer, providing necessary inflammatory signals, while initiating feedback suppression in both immune and.