Type I interferon response in the central nervous system

Stolzmann, Paul; Ricour, Céline; Sommereyns, Caroline; Sorgeloos, Frédéric; Michiels, Thomas

doi:10.1016/j.biochi.2007.02.009

Cited by 86 publications

(94 citation statements)

References 103 publications

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“…Type I IFNs are critical mediators of host immune responses in the CNS and participants in neurological disease pathogenesis (for review, see Paul et al, 2007). Chronically elevated levels of IFN-␣ in the CNS in CVE (Dussaix et al, 1985), AGS (Lebon et al, 1988b;Rice et al, 2007), and Cree encephalitis (Black et al, 1988) are linked to neurodegeneration, inflammation, and calcification.…”

Section: Discussionmentioning

confidence: 99%

The Type I Interferon-α Mediates a More Severe Neurological Disease in the Absence of the Canonical Signaling Molecule Interferon Regulatory Factor 9

Höfer¹,

Li²,

Lim³

et al. 2010

J. Neurosci.

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Section: Discussionmentioning

confidence: 99%

The Type I Interferon-α Mediates a More Severe Neurological Disease in the Absence of the Canonical Signaling Molecule Interferon Regulatory Factor 9

Höfer¹,

Li²,

Lim³

et al. 2010

J. Neurosci.

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“…Prolonged treatment with IFN results in psychiatric side effects including confusion, manic condition, sleep disturbance and a syndrome characteristic of depression (Paul et al, 2007;Raison et al, 2005). This behavioral response is possibly elicited by an amplification of the actions of other existing pro-inflammatory cytokines, much as described above for IL-6.…”

Section: Interferons (Ifns) and Behaviormentioning

confidence: 97%

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

McCusker

Kelley

2013

Journal of Experimental Biology

354

259

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Sickness and depressionOver the past 30years, it has become clear that the immune system plays a critical role in animal behavior. This role is tightly linked to the obvious role that immune cell activation plays in the clearance of pathogenic organisms. Systemic or central infections elicit a group of symptoms that are necessary for the organism to conserve resources, reorganize priorities and limit the spread of the infection to other members of the community. This sickness behavior is a motivational state that is common to most pathogeninduced infections ranging from viruses to multicellular parasites, but, because of its ubiquitous nature, is frequently accepted as an unavoidable and non-specific consequence of infection. However, considering the broad spectrum of symptoms -fever, nausea, decreased appetite, malaise, fatigue and achiness -it seems clear that a highly organized, although not pathogen-specific, response is being manifested to aid in the fight against infection (Dantzer, 2001;Ericsson et al., 1995).We are all familiar with the human symptoms of sickness but, to investigate changes in behavior associated with sickness, it is critical to have reliable animal measurements that relate to changes in the affective state. Using preclinical animal models, sickness behavior is best evaluated when the test involves a means to assess motivation. Sickness behavior is frequently assessed as social exploration/investigation (in rodent models, this response is frequently reported as a decrease in time actively seeking interaction with a novel animal as a result of diminished motivation for social exploration or neophobia). Social exploration is a naturalistic behavior and all animals have a strong motivation, whether driven by curiosity or sexual desire. With this strong motivational stimulus, infections cause a strong differential between time of exploration of healthy and sick animals, with less time of exploration being observed with sick animals. Another simpler but effective model is exploration of the environment [often referred to as locomotor activity (LMA), representing some level of physical movement in a novel environment such as rearing, quadrant entry, line crossings or total distance traveled; all of which are highly correlated]. LMA is best conducted in a novel environment, as the motivation to explore is stronger in this

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“…TLRs signal through the adaptor molecules, myeloid differentiation primary response gene 88 (MyD88) and Trif, to initiate intracellular signaling by transcription factors such as and the IFN regulatory factors (IRFs) (Alexopoulou et al, 2001). These IRFs are translocated to the host cell nucleus where they regulate inflammatory cytokine synthesis and stimulate type I interferon synthesis (IFN -expression) to produce a protective response (anti-viral state) in adjacent uninfected cells (Paul et al, 2007). A further anti-viral property of the IRF is through its binding to the pro-apoptotic protein Bax and translocation to the mitochondria with activation of the mitochondrial apoptotic pathway, terminating virus replication (Chattopadhyay et al, 2010).…”

Section: Tlrsmentioning

confidence: 99%

“…Indeed, CNS virus infections are more lethal in mice deficient in IFNAR than the wild type equivalent, emphasizing the importance of IFN/IFNAR pathway for anti-viral defense (Griffin, 2003;Paul et al, 2007). The type 1 interferon response is made by most CNS cells and results in a non-apoptotic anti-viral response by the host cell reducing infection by a replicating RNA virus (Katze et al, 2002).…”

Section: Cns Innate Immune System; Interferon Type 1 and 2 Responses mentioning

confidence: 99%

“…Host CNS cells in response to IFN stimulation produces a range of anti-viral ISGs, including oligoadenylate synthetase (OAS) and IFN-inducible ds RNAdependent protein kinase (PKR) that both modulate virus replication; RNAse L and Mx that inhibit viral transcription together with the RNA deaminases (ADAR-1 and APOBEC3G) producing mutations in viral genomes (Goodbourn et al, 2000) (George et al, 2009) . (IRFs) IRF-7, IRF-9, and ISG54 are all increased following CNS virus infection and one IRF, ISG15, has been found to be significantly increased in astrocytes following their infection with RNA virus (Paul et al, 2007). Type 2 interferon response is due to the interferon  again a glycoprotein expressed by activated T cells when TCR binds to their cognate antigen (Goodbourn et al, 2000).…”

Section: Cns Innate Immune System; Interferon Type 1 and 2 Responses mentioning

confidence: 99%

See 1 more Smart Citation

Virus-Induced Encephalitis and Innate Immune Responses – A Focus on Emerging or Re-Emerging Viruses

Denizot¹,

Thon-Hon²,

Kumar³

et al. 2011

Non-Flavivirus Encephalitis

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Type I interferon response in the central nervous system

Cited by 86 publications

References 103 publications

The Type I Interferon-α Mediates a More Severe Neurological Disease in the Absence of the Canonical Signaling Molecule Interferon Regulatory Factor 9

The Type I Interferon-α Mediates a More Severe Neurological Disease in the Absence of the Canonical Signaling Molecule Interferon Regulatory Factor 9

Immune–neural connections: how the immune system’s response to infectious agents influences behavior

Virus-Induced Encephalitis and Innate Immune Responses – A Focus on Emerging or Re-Emerging Viruses

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