Interferons

Maeyer, Edward De; Maeyer‐Guignard, Jaqueline De

doi:10.1007/978-1-4613-3009-7_5

Cited by 74 publications

(73 citation statements)

References 381 publications

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“…Proteins of the IRF family have been shown to be involved in the regulation of the pleiotropic activities elicited by IFNs including the modulation of the immune response, in¯ammation, hematopoiesis, cell proliferation and di erentiation (De Maeyer and De Maeyer, 1988;Taniguchi et al, 1995). This family includes IRF-1, IRF-2, ICSBP, ISGF3g, the recently described ICSAT/Pip/LSIRF, IRF3 and v-IRF encoded by a non structural gene of the human herpes virus 8 (HHV-8) (Nguyen et al, 1997b).…”

Section: Introductionmentioning

confidence: 99%

Activation and repression of the 2-5A synthetase and p21 gene promoters by IRF-1 and IRF-2

et al. 1999

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Section: Introductionmentioning

confidence: 99%

Activation and repression of the 2-5A synthetase and p21 gene promoters by IRF-1 and IRF-2

et al. 1999

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“…[1][2][3] NOD mice spontaneously develop autoimmune insulindependent diabetes mellitus (IDDM). 4,5 Islets of Langerhans are infiltrated by T cells, macrophages and other lymphoid cells (insulitis), and beta islet cells are selectively destroyed.…”

Section: Introductionmentioning

confidence: 99%

Prevention of autoimmune diabetes by intramuscular gene therapy with a nonviral vector encoding an interferon-gamma receptor/IgG1 fusion protein

Prud’homme

Chang

1999

Gene Ther

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We report on long-term delivery of an interferon-␥ (IFN␥) exceeding 100 ng/ml for months after treatment. These levinhibitory protein by intramuscular (i.m.) gene therapy. els are sufficient to neutralize IFN␥ in vivo, and to prevent IFN␥ is a cytokine that plays an important role in many either MDSD or cyclophosphamide (CYP)-accelerated inflammatory disorders, including autoimmune insulindiabetes in NOD mice, which are both characterized by dependent diabetes mellitus (IDDM) in NOD mice and (in systemic release of IFN␥. In these diseases gene therapy various strains) multiple low-dose streptozotocin (STZ)-considerably reduces inflammation in the islets of Langerinduced diabetes (MDSD). By cDNA insertion into plasmid hans (insulitis). Also, circulating IFN␥R/IgG1 blocked IFN␥-VICAL VR-1255 we constructed an expression vector enhanced nitric oxide production by peritoneal macroencoding a soluble IFN␥ receptor/IgG1 heavy chain (all phages. The fusion protein is constructed from nonmurine) fusion protein (IFN␥R/IgG1). This protein is immunogenic self elements, avoiding a neutralizing secreted as a homodimer and neutralizes IFN␥ in vitro. We immune response and making it suitable for prolonged show that i.m. injections of this vector as naked DNA in therapy of numerous inflammatory disorders. mice results in secretion of IFN␥R/IgG1, with serum levels

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“…The resistance of mice to infection by a particular virus may be a manifestation of lack of a receptor for virus attachment, inappropriate intracellular processing and replication, or failure of virus assembly or release, and may reflect genetically controlled responses (for reviews, see Brinton & Nathanson, 1981;Brinton et al, 1983). Furthermore, lymphokines, such as interferon, influence the replication of numerous viruses (De Maeyer & De Maeyer-Guignard, 1979;Hailer et al, 1981), including a strain of murine coronavirus (Virelizier, 1981).…”

Section: Introductionmentioning

confidence: 99%

Host Genetic Control of Mouse Hepatitis Virus Type 4 (JHM Strain) Replication. I. Restriction of Virus Amplification and Spread in Macrophages from Resistant Mice

Knobler

Tunison

Oldstone

1984

Journal of General Virology

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SUMMARYPeritoneal macrophages were used to analyse host genetic control of mouse hepatitis virus type 4 (MHV-4) infection. Both infectious centre and immunofluorescence assays indicated that only a subset of macrophages from either susceptible (BALB, C3H or C57BL/6J) or resistant (SJL/J) mice were initially infected with MHV-4 during the first cycle of infection. However, compared to macrophages from susceptible mice, three-to sixfold fewer SJL/J macrophages were infected, and there was no amplification of virus replication by involvement of adjacent cells during the second cycle of infection. Treatment of macrophages from susceptible mice with interferon beta could not duplicate the aborted second cycle of infection that occurred in macrophages from resistant mice.

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Interferons

Cited by 74 publications

References 381 publications

Activation and repression of the 2-5A synthetase and p21 gene promoters by IRF-1 and IRF-2

Activation and repression of the 2-5A synthetase and p21 gene promoters by IRF-1 and IRF-2

Prevention of autoimmune diabetes by intramuscular gene therapy with a nonviral vector encoding an interferon-gamma receptor/IgG1 fusion protein

Host Genetic Control of Mouse Hepatitis Virus Type 4 (JHM Strain) Replication. I. Restriction of Virus Amplification and Spread in Macrophages from Resistant Mice

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