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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

Authors
 Jin-Won Seo  ;  Eun-Jeong Yang  ;  Se Hoon Kim  ;  In-Hong Choi 
Citation
 BMB Reports, Vol.48(12) : 696-701, 2015 
Journal Title
 BMB Reports 
ISSN
 1976-6696 
Issue Date
2015
MeSH
Alternative Splicing ; Astrocytes/drug effects ; Astrocytes/immunology ; Astrocytes/metabolism* ; Cell Line, Tumor ; Down-Regulation ; Encephalitis/genetics ; Encephalitis/immunology ; Encephalitis/metabolism ; Humans ; Interferon Regulatory Factor-3/antagonists & inhibitors ; Interferon Regulatory Factor-3/immunology ; Interferon-alpha/immunology ; Interferon-alpha/pharmacology* ; Interferon-beta/immunology ; Interferon-beta/pharmacology ; Poly I-C/pharmacology ; Protein Isoforms ; RNA, Double-Stranded ; Signal Transduction ; Toll-Like Receptor 3/biosynthesis* ; Toll-Like Receptor 3/genetics ; Toll-Like Receptor 3/immunology
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/interferon-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 Bα 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.
Files in This Item:
T201505160.pdf Download
DOI
10.5483/BMBRep.2015.48.12.106
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Se Hoon(김세훈) ORCID logo https://orcid.org/0000-0001-7516-7372
Seo, Jin Won(서진원)
Choi, In Hong(최인홍) ORCID logo https://orcid.org/0000-0001-9851-0137
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/157046
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