Literature DB >> 30439714

Type III Interferons in Viral Infection and Antiviral Immunity.

Jian-Hua Zhou1, Yi-Ning Wang2, Qiu-Yan Chang3, Peng Ma3, Yonghao Hu2, Xin Cao2,3.   

Abstract

Interferons (IFNs) can serve as the first line of immune defense against viral infection. The identification of IFN-λs 1, 2, 3 & 4 (termed as type III IFNs) has revealed that the antiviral immune response to viruses contains more components than the type I IFNs that have been known for more than 50 years. IFN-λs are IFN-λ1 (IL-29), IFN-λ2 (IL-28a), IFN-λ3 (IL-28b) and IFN-λ4, which resembles IFN-λ3. IFN-λs have type I-IFN-like immune responses and biological activities, but our knowledge of these novel players in the antiviral response is not well established. In this review, we try to describe the current information on the expression and function of IFN-λs in the innate antiviral immune defense and IFN-λ2's role in regulating and shaping the adaptive immune response. We suggest that IFN-λs are key antiviral cytokines, directly performing an antiviral immune response at epithelial surfaces in the early stages of viral infection, and that these cytokines also skew the balance of Th1 and Th2 cells to Th1 phenotype. In addition, genetic polymorphisms in IFN-λ genes can impair antiviral immune responses in clinical treatment.
© 2018 The Author(s). Published by S. Karger AG, Basel.

Entities:  

Keywords:  Adaptive immune; Cytokine; Immune defense; Innate immune; Interferon; Viral infection

Mesh:

Substances:

Year:  2018        PMID: 30439714     DOI: 10.1159/000495172

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  47 in total

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2.  LYAR Suppresses Beta Interferon Induction by Targeting Phosphorylated Interferon Regulatory Factor 3.

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4.  Mutations in Porcine Epidemic Diarrhea Virus nsp1 Cause Increased Viral Sensitivity to Host Interferon Responses and Attenuation In Vivo.

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Review 9.  Type I Interferon-Mediated Regulation of Antiviral Capabilities of Neutrophils.

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Review 10.  Review of studies of severe acute respiratory syndrome related coronavirus-2 pathogenesis in human organoid models.

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