IFN-<i>λ</i>: A New Class of Interferon with Distinct Functions-Implications for Hepatitis C Virus Research

Liu, Bing; McGilvray, Ian

doi:10.1155/2015/796461

Cited by 8 publications

(6 citation statements)

References 86 publications

(85 reference statements)

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“…IL-28B acted synergically with more mature NK cells to defend against influenza virus to elicit the greatest protective effect. Type I IFN produced severe side effects in clinical trials (18), and type III IFN is expected to elicit reduced side effects because its receptor is expressed on limited cell types. In our experiments, mice overexpressing IL-28B exhibited relatively normal growth.…”

Section: Discussionmentioning

confidence: 99%

“…IFN-l has received increasing attention in clinical studies because of its roles in defending against hepatitis C virus (HCV) and hepatitis B virus infections (14)(15)(16). Single-nucleotide polymorphisms linked to IL-28B are associated with a lower response to IFN-based therapy in patients with HCV infection (17,18). Encouraging results for the treatment of HCV infection have been observed in IFN-l phase III clinical trials (19).…”

Section: Involvement Of Nk Cells In Il-28b-mediated Immunity Against mentioning

confidence: 99%

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Involvement of NK Cells in IL-28B–Mediated Immunity against Influenza Virus Infection

Wang

Chen

et al. 2017

The Journal of Immunology

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IL-28B is a member of the newly discovered type III IFN family and exhibits unique antiviral properties compared with other family members. NK cells play a critical role in defending against viruses; however, little is known about the role of IL-28B in NK cell function. In a mouse model of influenza A virus (mouse adapted influenza A/PR/8/34 strain) infection, long-term overexpression of IL-28B induced by hepatocyte-specific gene delivery exerted a strong antiviral effect in the presence of NK cells. In IL-28B-overexpressing wild-type mice, the percentages and absolute numbers of NK cells in the spleen, liver, and lung were markedly increased, with higher proliferation and accelerated NK cell maturation based on phenotypes staining with CD11b and CD27 or CD11b and KLRG1. Furthermore, the effect of IL-28B on NK cells was macrophage dependent, as confirmed in an in vitro coculture assay and in in vivo macrophage- or alveolar macrophage-depletion experiments. Transwell studies demonstrated that CFSE-labeled NK cell proliferation was driven, in a dose-dependent manner, by unknown soluble factor(s) secreted by IL-28B-stimulated alveolar macrophages, without requiring direct cell-cell contact. An understanding of the NK cell-promoting features of IL-28B will facilitate future clinical application of this cytokine.

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Section: Discussionmentioning

confidence: 99%

Section: Involvement Of Nk Cells In Il-28b-mediated Immunity Against mentioning

confidence: 99%

Involvement of NK Cells in IL-28B–Mediated Immunity against Influenza Virus Infection

Wang

Chen

et al. 2017

The Journal of Immunology

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“…IL-28B belongs to type III IFN. IL-28B shows potential advantage in use when compared with Type I IFN as Type I IFN showed severe side effects in clinical trials 30 . In our study, mice administrated with IL-28B through hydrodynamic injection were relatively normal because IL-28R is expressed on limited cell types.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-28B dampens protease-induced lung inflammation via IL-25 and TSLP inhibition in epithelial cells

Yan

Gao

Guo

et al. 2020

Sci Rep

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Asthma is a chronic respiratory disease with high heterogeneity in human. Different mouse models have been applied for investigation of pathogenesis and treatment of asthma, which target on different cells, receptors and pathways. Interleukin (IL-) 28B, a member of λ-interferons, have been shown to play a protective role in OVA-induced asthma, which is antigen-specific and adaptive immune system dominant. However, the roles of IL-28B in protease-induced asthma, an adaptive immune system independent asthma, are still unclear. Here, we used plant-derived cysteine protease, papain to induce asthma in mice and found that IL-28B was capable of alleviating papain-induced asthma. Papain challenge lead to activation of epithelial cells and production of alarmin, such as IL-25 and thymic stromal lymphopoietin and IL-28B treatment down-regulated their production. Further mechanism was proved to be that IL-28B inhibited the phosphorylation of Erk in epithelial cells via interaction with their receptors. Our results reveal a protective role of IL-28B via regulation of epithelial cells in protease induced asthma.

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“…Indeed, it has been reported that pegylated IFN‐λ used as a treatment in patients with chronic hepatitis B can activate robust innate and adaptive antiviral responses in vivo (Phillips et al, 2017). Interestingly, several publications have also investigated the role of IFN‐λ during HCV infection, particularly in regard to the association between IFN‐λ3 polymorphisms and reduced viral clearance and response to interferon‐based treatment (Boisvert & Shoukry, 2016; Bruening et al, 2017; Liu et al, 2015; Scagnolari et al, 2017).…”

Section: Dysfunctional Immunity In Alcoholic Liver Disease: Lessons L...mentioning

confidence: 99%

A review of alcohol–pathogen interactions: New insights into combined disease pathomechanisms

Osna

New-Aaron

Dagur

et al. 2022

Alcoholism Clin & Exp Res

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Progression of chronic infections to end‐stage diseases and poor treatment results are frequently associated with alcohol abuse. Alcohol metabolism suppresses innate and adaptive immunity leading to increased viral load and its spread. In case of hepatotropic infections, viruses accelerate alcohol‐induced hepatitis and liver fibrosis, thereby promoting end‐stage outcomes, including cirrhosis and hepatocellular carcinoma (HCC). In this review, we concentrate on several unexplored aspects of these phenomena, which illustrate the combined effects of viral/bacterial infections and alcohol in disease development. We review alcohol‐induced alterations implicated in immunometabolism as a central mechanism impacting metabolic homeostasis and viral pathogenesis in Simian immunodeficiency virus/human immunodeficiency virus infection. Furthermore, in hepatocytes, both HIV infection and alcohol activate oxidative stress to cause lysosomal dysfunction and leakage and apoptotic cell death, thereby increasing hepatotoxicity. In addition, we discuss the mechanisms of hepatocellular carcinoma and tumor signaling in hepatitis C virus infection. Finally, we analyze studies that review and describe the immune derangements in hepatotropic viral infections focusing on the development of novel targets and strategies to restore effective immunocompetency in alcohol‐associated liver disease. In conclusion, alcohol exacerbates the pathogenesis of viral infections, contributing to a chronic course and poor outcomes, but the mechanisms behind these events are virus specific and depend on virus–alcohol interactions, which differ among the various infections.

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IFN-λ: A New Class of Interferon with Distinct Functions-Implications for Hepatitis C Virus Research

Cited by 8 publications

References 86 publications

Involvement of NK Cells in IL-28B–Mediated Immunity against Influenza Virus Infection

Involvement of NK Cells in IL-28B–Mediated Immunity against Influenza Virus Infection

Interleukin-28B dampens protease-induced lung inflammation via IL-25 and TSLP inhibition in epithelial cells

A review of alcohol–pathogen interactions: New insights into combined disease pathomechanisms

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