ISG56 is involved in CXCL10 expression induced by TLR3 signaling in BEAS-2B bronchial epithelial cells

Shiratori, Toshihiro; Imaizumi, Tadaatsu; Hirono, Koji; Kawaguchi, Shogo; Matsumiya, Tomoh; Seya, Kazuhiko; Tasaka, Sadatomo

doi:10.1080/01902148.2020.1760965

Cited by 9 publications

(9 citation statements)

References 31 publications

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“…ISG56 protein expression was not found in unstimulated BEAS-2B, and poly I:C treatment significantly upregulated ISG56 protein expression as previously reported. 12 Effective knockdown of ISG56 protein upon siRNA transfection was further confirmed in Western blot analysis (Figure 4(b)).…”

Section: Resultsmentioning

confidence: 67%

“…There are various antiviral mediators in the ISGs pathway, which exert antiviral effects through their complex interactions. 17 In a prior research, Shiratori et al 12 showed that the TLR3/IFN-β/ISG56/CXCL10 axis in BEAS-2B cells. Therefore, the relationship between ISG56 and IFITM1 was investigated in this study.…”

Section: Discussionmentioning

confidence: 98%

“…[9][10][11] ISG56 was also found to function for defense against infection of viruses in bronchial epithelial cells. 12 BEAS-2B are cell line of non-cancerous human bronchial epithelial cells, 13 which provides a proper model for investigating innate immunity. ISG56 is induced by polyinosinic-polycytidylic acid (poly I:C), an activator of TLR3, and enhances CXCL10 expression in BEAS-2B.…”

Section: Impact Statementmentioning

confidence: 99%

“…ISG56 is induced by polyinosinic-polycytidylic acid (poly I:C), an activator of TLR3, and enhances CXCL10 expression in BEAS-2B. 12 However, it remains unclear whether IFITM1 is expressed in bronchial epithelial cells via TLR3 activation. In this study, IFITM1 expression was investigated in BEAS-2B cells incubated with poly I:C. Moreover, it was examined whether IFN-β and/ or ISG56 are associated with inducing poly I:C-mediated IFITM1 expression.…”

Section: Impact Statementmentioning

confidence: 99%

“…9 –11 ISG56 was also found to function for defense against infection of viruses in bronchial epithelial cells. 12…”

Section: Introductionmentioning

confidence: 99%

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Toll-like receptor 3 signaling induces interferon-induced transmembrane protein 1 in BEAS-2B cells

Dobashi

Shiratori

Imaizumi

et al. 2022

Exp Biol Med (Maywood)

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The human bronchial epithelium plays a crucial role in mediating antiviral immune reactions. When double-stranded RNA (dsRNA) binds to the receptor named Toll-like receptor (TLR) 3, activation of antiviral innate immune reactions is initiated by producing interferon (IFN) type I. Then, type I IFN promotes the transcription of IFN-stimulated genes (ISGs). Proteins encoded by ISGs reveal antiviral effects. The IFN-induced transmembrane protein 1 (IFITM1) is an ISG family member that inhibits viral infection by preventing the entry of viruses with a cell membrane. However, IFITM1 expression in human bronchial epithelium remains largely undetermined. Here, we investigated whether IFITM1 is expressed in cultured BEAS-2B bronchial epithelial cells. Polyinosinic:polycytidylic acid (poly I:C) was used for treatment of BEAS-2B as a TLR3 ligand. IFITM1 expression levels were measured using reverse transcription–quantitative PCR and Western blotting. Using RNA interference, we determined the significance of IFN-β and ISG56 on IFITM1 upregulation. Poly I:C treatment significantly upregulated IFITM1 expression in BEAS-2B cells, and it was concentration- and time-dependent. Knockdown of IFN-β or ISG56 decreased poly I:C-induced IFITM1 expression levels. Recombinant IFN-β also increased expression levels of IFITM1. In BEAS-2B cells, IFITM1 expression is upregulated by poly I:C, at least partly, via the TLR3/IFN-β/ISG56 axis. Thus, IFITM1 may contribute to antiviral innate immunity in bronchial epithelium.

show abstract

Section: Resultsmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 98%

Section: Impact Statementmentioning

confidence: 99%

Section: Impact Statementmentioning

confidence: 99%

“…9 –11 ISG56 was also found to function for defense against infection of viruses in bronchial epithelial cells. 12…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Toll-like receptor 3 signaling induces interferon-induced transmembrane protein 1 in BEAS-2B cells

Dobashi

Shiratori

Imaizumi

et al. 2022

Exp Biol Med (Maywood)

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TMEM2 suppresses TLR3-mediated IFN-β/ISG56/CXCL10 expression in BEAS-2B bronchial epithelial cells

Kobori,

Tachizaki,

Imaizumi

et al. 2024

Mol Biol Rep

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The molecular language of RNA 5′ ends: guardians of RNA identity and immunity

Avila-Bonilla,

Macias

2024

RNA

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RNA caps are deposited at the 5’end of RNA-polymerase II transcripts. This modification regulates several steps of gene expression, in addition to marking transcripts as self to enable the innate immune system to distinguish them from uncapped foreign RNAs, including those derived from viruses. Specialized immune sensors, such as RIG-I and IFITs, trigger antiviral responses upon recognition of uncapped cytoplasmic transcripts. Interestingly, uncapped transcripts can also be produced by mammalian hosts. For instance, 5'-triphosphate RNAs are generated by RNA-polymerase III transcription, including tRNAs, Alu RNAs, or vault RNAs. These RNAs have emerged as key players of innate immunity, as they can be recognised by the antiviral sensors. Mechanisms that regulate the presence of 5-triphosphates, such as 5' end dephosphorylation or RNA editing, prevent immune recognition of endogenous RNAs and excessive inflammation. Here, we provide a comprehensive overview of the complexity of RNA cap structures and 5'-triphosphate RNAs, highlighting their roles in transcript identity, immune surveillance, and disease.

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ISG56 is involved in CXCL10 expression induced by TLR3 signaling in BEAS-2B bronchial epithelial cells

Cited by 9 publications

References 31 publications

Toll-like receptor 3 signaling induces interferon-induced transmembrane protein 1 in BEAS-2B cells

Toll-like receptor 3 signaling induces interferon-induced transmembrane protein 1 in BEAS-2B cells

TMEM2 suppresses TLR3-mediated IFN-β/ISG56/CXCL10 expression in BEAS-2B bronchial epithelial cells

The molecular language of RNA 5′ ends: guardians of RNA identity and immunity

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