An inhibitory alternative splice isoform of Toll-like receptor 3 is induced by type I interferons in human astrocyte cell lines

Jin Won Seo, Eun Jeong Yang, SeHoon Kim, In Hong Choi

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Toll-like receptor 3 (TLR3) recognizes viral double-stranded RNA. It stimulates pro-inflammatory cytokine and interferon production. Here we reported the expression of a novel isoform of TLR3 in human astrocyte cell lines whose message is generated by alternative splicing. The isoform represents the N-terminus of the protein. It lacks many of the leucine-rich repeat domains, the transmembrane domain, and the intracellular Toll/interleukin-1 receptor domain of TLR3. Type I interferons (interferon-α and interferon-β) induced the expression of this isoform. Exogenous overexpression of this isoform inhibited interferon regulatory factor 3, signal transducers and activators of transcription 1, and Inhibitor of kappa B α signaling following stimulation. This isoform of TLR3 also inhibited the production of chemokine interferon-γ-inducible protein 10. Our study clearly demonstrated that the expression of this isoform of TLR3 was a negative regulator of signaling pathways and that it was inducible by type I interferons. We also found that this isoform could modulate inflammation in the brain.

Original languageEnglish
Pages (from-to)696-701
Number of pages6
JournalBMB reports
Volume48
Issue number12
DOIs
Publication statusPublished - 2015 Jan 1

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Toll-Like Receptor 3
Interferon Type I
Astrocytes
Protein Isoforms
Cells
Cell Line
Interferons
Interferon Regulatory Factor-3
Chemokine CXCL10
STAT1 Transcription Factor
Interleukin-1 Receptors
Double-Stranded RNA
Viral RNA
Alternative Splicing
Encephalitis
Chemokines
Leucine
Brain
Cytokines

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Cite this

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abstract = "Toll-like receptor 3 (TLR3) recognizes viral double-stranded RNA. It stimulates pro-inflammatory cytokine and interferon production. Here we reported the expression of a novel isoform of TLR3 in human astrocyte cell lines whose message is generated by alternative splicing. The isoform represents the N-terminus of the protein. It lacks many of the leucine-rich repeat domains, the transmembrane domain, and the intracellular Toll/interleukin-1 receptor domain of TLR3. Type I interferons (interferon-α and interferon-β) induced the expression of this isoform. Exogenous overexpression of this isoform inhibited interferon regulatory factor 3, signal transducers and activators of transcription 1, and Inhibitor of kappa B α signaling following stimulation. This isoform of TLR3 also inhibited the production of chemokine interferon-γ-inducible protein 10. Our study clearly demonstrated that the expression of this isoform of TLR3 was a negative regulator of signaling pathways and that it was inducible by type I interferons. We also found that this isoform could modulate inflammation in the brain.",
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An inhibitory alternative splice isoform of Toll-like receptor 3 is induced by type I interferons in human astrocyte cell lines. / Seo, Jin Won; Yang, Eun Jeong; Kim, SeHoon; Choi, In Hong.

In: BMB reports, Vol. 48, No. 12, 01.01.2015, p. 696-701.

Research output: Contribution to journalArticle

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