Anti-inflammatory properties of Type I interferons

Billiau, Alfons

doi:10.1016/j.antiviral.2006.03.006

Cited by 78 publications

(68 citation statements)

References 81 publications

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“…The immunomodulatory functions of IFN-I have been increasingly attracting attention in recent years (43)(44)(45). One manifestation of their immunomodulatory potential is that IFN-I promotes the expression of IL-10, which has been shown in both mouse and human APCs (46,47).…”

Section: Discussionmentioning

confidence: 99%

Type I IFN Inhibits Innate IL-10 Production in Macrophages through Histone Deacetylase 11 by Downregulating MicroRNA-145

Lin

Hou

et al. 2013

The Journal of Immunology

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Innate immune responses must be tightly regulated to avoid overactivation and subsequent inflammatory damage to host tissue while eliminating invading pathogens. IL-10 is a crucial suppressor of inflammatory responses and its expression is under precise regulation involving complex regulatory networks and multiple feedback loops. MicroRNAs are now emerging as critical regulators in immune response. Our previous work showed that miR-143/145 cluster was markedly downregulated in macrophages upon vesicular stomatitis virus infection. However, the particular role of miR-143/145 cluster in the regulation of innate immune response remains unknown. In this study, we found that miR-143/145 cluster expression was also downregulated dramatically by TLR signals in macrophages, which was dependent on the subsequent type I IFN (IFN-I) production and downstream IFN-I receptor–JAK1–STAT1 signal cascade. Further studies demonstrated that miR-145, but not miR-143, promoted IL-10 expression in TLR4-triggered macrophages through directly targeting the epigenetic Il10 gene silencer histone deacetylase 11. Therefore, we demonstrate that miR-145, downregulated by IFN-I, targets histone deacetylase 11 to promote innate IL-10 expression in macrophages. Our findings suggest a new IFN-I–mediated negative feedback loop in the fine-tuning of innate IL-10 production that creates precise coordination of innate immune responses.

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Section: Discussionmentioning

confidence: 99%

Type I IFN Inhibits Innate IL-10 Production in Macrophages through Histone Deacetylase 11 by Downregulating MicroRNA-145

Lin

Hou

et al. 2013

The Journal of Immunology

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“…This leads to the production of type I IFNs (IFN-␣␤), which bind to the type I IFN receptor (IFNAR) to activate the JAK-STAT signaling pathway, resulting in the up-regulation of antiviral genes (11). In addition to their antiviral activities, type I IFNs appear to possess potent anti-inflammatory properties and have been used to treat autoimmune disease such as multiple sclerosis (12)(13)(14). The mechanism responsible for these anti-inflammatory effects is thought to be related to type I IFN-induced IL-10 production, although this premise has remained controversial due to conflicting data (13,(15)(16)(17).…”

mentioning

confidence: 99%

Cutting Edge: Involvement of the Type I IFN Production and Signaling Pathway in Lipopolysaccharide-Induced IL-10 Production

Chang

Guo

Doyle

et al. 2007

The Journal of Immunology

206

184

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Macrophages respond to LPS by the rapid activation of proinflammatory cytokines that serve to initiate host defense against microbial invasion. To prevent injury to the host from excess production of these cytokines, IL-10 is up-regulated to feedback inhibit the proinflammatory response. However, the molecular events responsible for LPS-induced up-regulation of IL-10 remain to be elucidated. In this study, we provide evidence that production of and signaling by type I IFN is required for LPS-induced IL-10 up-regulation. In addition, we demonstrate that defect in type I IFN production and signaling results in a trend toward LPS-mediated superinduction of proinflammatory genes and cytokines in bone marrow-derived macrophages. Our findings suggest a novel anti-inflammatory role for the type I IFN production and signaling pathway in regulating LPS response in bone marrow-derived macrophages.

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“…Interestingly, it has been known for some time that components of the type I interferon pathway are in fact immunosuppressive . This is also the basis of the use of type I IFNs for the treatment of multiple sclerosis (Comabella et al 2002;Billiau 2006). Very interestingly, production of both IFN-β and IL-10 share a common pathway when activated by TLR signalling (Hacker et al 2006;Chang et al 2007).…”

Section: Exploitation Of Lentivirally Transduced Dendritic Cells For mentioning

confidence: 99%

Dendritic Cells and Lentiviral Vectors: Mapping the Way to Successful Immuno Gene Therapy

Goyvaerts¹,

Kochan²,

Escors³

et al. 2011

Viral Gene Therapy

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Anti-inflammatory properties of Type I interferons

Cited by 78 publications

References 81 publications

Type I IFN Inhibits Innate IL-10 Production in Macrophages through Histone Deacetylase 11 by Downregulating MicroRNA-145

Type I IFN Inhibits Innate IL-10 Production in Macrophages through Histone Deacetylase 11 by Downregulating MicroRNA-145

Cutting Edge: Involvement of the Type I IFN Production and Signaling Pathway in Lipopolysaccharide-Induced IL-10 Production

Dendritic Cells and Lentiviral Vectors: Mapping the Way to Successful Immuno Gene Therapy

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