[23] Induction of rat interferon in vivo and in vitro—physicochemical and biological characterization

Poindron, Philippe; Coupin, G.; Illinger, Dominique; Fauconnier, B

doi:10.1016/0076-6879(81)78113-8

Cited by 9 publications

(5 citation statements)

References 8 publications

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“…Since there is little or no expression of MHC antigens on normal CNS cells (8), it might be expected that virally infected brain cells could escape recognition and destruction by cytotoxic T cells, which can recognize viral antigens only in association with cellular MHC antigens (44). Since CNS cells show enhanced expression of MHC antigens in response to IFN, and the peripheral IFN classes (a, ~, and 7) do not appear to cross the blood-brain barrier (5,22,30,35), IFN produced by astrocytes may play an important role in CNS immune responses by enhancing the expression of MHC antigens on previously immunologically incompetent brain cells, which then become competent to participate in T cellmediated responses. This mechanism may contribute to CNS degenerative diseases such as multiple sclerosis, where T cells infiltrate the CNS (7,38).…”

Section: Discussionmentioning

confidence: 99%

“…Since H-2 antigens have a critical role in immune responses, astrocyte IFN may initiate and participate in immune reactions that contribute to immunoprotective and immunopathological responses in the CNS. T HE central nervous system (CNS) 1 has classically been thought to be an immunologically privileged site in that: (a) it lacks lymphatic drainage (32); (b) the CNS cells express low levels of antigens encoded by the major histocompatibility complex (MHC) which function to both initiate and effect immune responses (8,20); and (c) it is protected by the blood-brain barrier which is impermeable to many substances, including the known classes of interferons (IFN a, ~, and 3') (5,22,30,35).…”

mentioning

confidence: 99%

“…IFN-3, modulation of MHC antigens on neurons and/or glia might enable normally sequestered immunoincompetent cells of the brain to participate in T cell-mediated responses, and may play an important role for brain diseases that have an immunological component. However, this cooperation of brain and immune cells appears to involve passage of T cells across the blood-brain barrier, so that they enter the brain and release lymphokines as IFN-3", which normally cannot pass the blood-brain barrier (5,22,30,35).…”

mentioning

confidence: 99%

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Astrocytes produce interferon that enhances the expression of H-2 antigens on a subpopulation of brain cells.

Tedeschi

Barrett

Keane

1986

The Journal of Cell Biology

139

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Abstract. Using primary culture methods, we show that purified astrocytes from embryonic mouse or rat central nervous system (CNS) can be induced to produce interferon (IFN) activity when pretreated with a standard IFN-superinducing regimen of polyribonucleotide, cycloheximide, and actinomycin D, whereas IFN activity was not inducible in neuronal cultures derived from mouse CNS. Astrocyte IFN displays inductive, kinetic, physicochemical, and antigenic prop-

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Astrocytes produce interferon that enhances the expression of H-2 antigens on a subpopulation of brain cells.

Tedeschi

Barrett

Keane

1986

The Journal of Cell Biology

139

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“…Since peripheral IFN ( a , p, y) do not appear to cross the blood-brain barrier (Billiau, 1981;Poindron et al, 1981), VIP-induced IFN could be a novel way by which brain cells respond to endogenous neurotransmitters. It may be speculated that IFN alp released by glial cells in response to VIP or poly (I).poly (C,,U) plays an important role in protecting the brain against viruses and in generating immune response in the CNS.…”

Section: Vip Induced 2'5'a Synthetase and Antiviralmentioning

confidence: 99%

Induction by vasoactive intestinal peptide of interferon α/β synthesis in glial cells but not in neurons

Chelbi-Alix

Brouard

Boissard

et al. 1994

Journal Cellular Physiology

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Vasoactive intestinal peptide (VIP), a 28-amino acid peptide, plays a multifunctional neuromodulatory role in both peripheral and central nervous systems. We have recently reported that VIP induces interferon (IFN) alpha/beta synthesis in human colon adenocarcinoma cell line HT-29. It has been reported that VIP may counteract HIV-induced neuronal cell death; therefore, we postulated that the action of VIP may be mediated by a cascade regulation, involving the production of some cytokines such as IFN. Here we demonstrate that primary cultures of rat mesencephalic neurons and glial cells respond differently to VIP. Thus VIP enhanced 2'5' oligoadenylate (2'5' A) synthetase activity and inhibited vesicular stomatitis virus multiplication in glial cultures only. However, both cell cultures had functional adenylate cyclase coupled receptors for VIP. The increase in 2'5'A synthetase activity in glial cultures reached a maximum with 10(-6) M VIP and required cellular RNA and protein synthesis. Anti-IFN alpha/beta, but not anti-IFN gamma, antibodies abolished the induction of the antiviral and 2'5'A synthetase activities by VIP in rat glial-enriched cultures, suggesting that these inductions were mediated through IFN alpha/beta synthesis. Moreover, VIP or poly (i). poly (C12U) caused, in the glial cultures, the induction and secretion of an IFN of type alpha/beta with a titer value of 16 and 32 units/ml respectively. In contrast, neither of these two substances was able to induce IFN synthesis in neurons, which were, however, sensitive to IFN alpha/beta produced by VIP-treated glial cells. IFN produced by VIP in glial cells may therefore play an important role in defending the brain against viruses.

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“…However, Anthony et al (33) have suggested that the effect of polyI/C, ABPP, and AIPP may act by non-IFN mechanisms in inducing Listeria protection. In addition, circulating IFN is found only in low concentration after these agents are administered to rats (34). To determine the importance of IFN-a/@ and IFN-y more precisely, studies were repeated using purified rat IFN-a/@, IFN-y, and rat rIFN-y.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Host Defense Mechanisms against Listeria monocytogenes Infection: The Role of Lipopolysaccharides and Interferons

Bortolussi¹,

Issekutz

Burbridge³

et al. 1989

Pediatr Res

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ABSTRACT. The human newborn infant is susceptible to lethal infection caused by a number of bacterial species including Listeria monocytogenes, a gram-positive rod which is pathogenic by virtue of its ability to survive intracellularly. In adult animals interferon (1FN)-alp and IFN-y or agents that induce or augment IFN production confer protection against lethal L. monocytogenes infection. Regulation and production of IFN is poorly understood during the neonatal period. We therefore evaluated the role of IFN-a/@ and IFN-y, IFN-inducers (po1yinosinic:polycytidylic acid, amino-bromo-phenyl-pyrimidinone, aminoiodophenyl pyrimidinone) and lipopolysaccharide in modifying neonatal L. monocytogenes infection. Pretreatment of juvenile rats with polyinosinic:polycytidylic acid or lipopolysaccharide protected them against a lethal challenge with L. monocytogenes. Among newborn rats, polyinosinic: polycytidylic acid, amino-iodo-phenyl pyrimidinone and amino-bromophenyl-pyrimidinone gave significant protection, however, lipopolysaccharide did not influence survival. The role of IFN was further examined. Pretreatment of 3-d-old rats with purified IFN-a/& native rat IFN-y or rDNA rat IFN-y protected them against the lethality of subsequent L. monocytogenes injection. At 3 d after bacterial challenge, bacterial content in the spleens of 3-d-old rats pretreated with rIFN-y were significantly decreased compared to controls: IFN-alp-pretreated animals had less of a decrease, which become significant only 5 d after challenge. Our experiments indicate a role for IFN in neonatal host defense against L. monocytogenes infection. (Pediatr Res 25:311-315, 1989) Abbreviations IFN, interferon polyI/C, polyinosinic:polycytidylic acid ABPP, amino-bromo-phenyl-pyrimidinone AIPP, amino-iodo-phenyl-pyrimidinone LPS, lipopolysaccharide CFU, colony forming units of bacteria ip, intraperitoneal sc, subcutaneous TNF, tumor necrosis factor

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[23] Induction of rat interferon in vivo and in vitro—physicochemical and biological characterization

Cited by 9 publications

References 8 publications

Astrocytes produce interferon that enhances the expression of H-2 antigens on a subpopulation of brain cells.

Astrocytes produce interferon that enhances the expression of H-2 antigens on a subpopulation of brain cells.

Induction by vasoactive intestinal peptide of interferon α/β synthesis in glial cells but not in neurons

Neonatal Host Defense Mechanisms against Listeria monocytogenes Infection: The Role of Lipopolysaccharides and Interferons

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