Evidence map›Paper›PMID 38923445›Full record

ArticleFEBS open bio2024

Interferon-stimulated gene 56 positively regulates Toll-like receptor 3-mediated CXCL10 expression in human renal proximal tubular epithelial cells.

Mayuki Tachizaki, Sho Sakamoto, Yuri Kobori, Yoshiya Asano, Shogo Kawaguchi, Kazuhiko Seya, Hiroshi Tanaka, Eiji Morita, Tadaatsu Imaizumi

Abstract read
In one paragraph

Article in FEBS open bio, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. A novel two-hit murine model of viral-primed sepsis-associated acute kidney injury.American journal of physiology. Renal physiology · 2026
    Article
  2. Article
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Mayuki TachizakiDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.ORCID 0009-0002-7343-9121
Sho SakamotoDepartment of Biochemistry and Molecular Biology, Hirosaki University Faculty of Agriculture and Life Science, Japan.
Yuri KoboriDepartment of Respiratory Medicine, Hirosaki University Graduate School of Medicine, Japan.
Yoshiya AsanoDepartment of Neuroanatomy, Cell Biology and Histology, Hirosaki University Graduate School of Medicine, Japan.
Shogo KawaguchiDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.ORCID 0000-0001-5599-1110
Kazuhiko SeyaDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.
Hiroshi TanakaDepartment of School Health Science, Hirosaki University Faculty of Education, Japan.
Eiji MoritaDepartment of Biochemistry and Molecular Biology, Hirosaki University Faculty of Agriculture and Life Science, Japan.
Tadaatsu ImaizumiDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Japan.

Funding

Japan Society for the Promotion of Science 22K07862
6 · The paper itself

Abstract

Viral infections in tubular epithelial cells lead to the production of inflammatory cytokines by innate immunity, causing tubulointerstitial nephritis. TLR3 recognizes viral infections and acts via the activation of interferon (IFN)/IFN-stimulated genes (ISGs). This study investigates the role of ISG56, a representative ISG, in TLR3 signaling in cultured human renal proximal tubular epithelial cells (hRPTECs). To this end, hRPTECs were stimulated by a synthetic TLR3 ligand, polyinosinic-polycytidylic acid (poly IC), recombinant human interferon-β [r(h)IFN-β] or Japanese encephalitis virus (JEV) infection and assayed for inflammatory cytokine mRNA expression by RT-qPCR, and protein expression via western blotting or ELISA. ISG56 was expressed by poly IC or r(h)IFN-β and IFN-β knockdown reduced poly IC-induced expression of ISG56 and CXCL10. Moreover, ISG56 knockdown reduced poly IC- or r(h)IFN-β-induced expression of CXCL10 at the same time as increasing JEV growth and reducing CXCL10 expression induced by JEV infection. Overall, TLR3 signaling induced IFN-β-dependent expression of ISG56 and CXCL10. We show that ISG56 possibly plays a critical role in antiviral immunity of hRPTECs by positive regulation of IFN-β-mediated CXCL10 expression downstream of TLR3.

Indexed as

Chemokine CXCL10Epithelial CellsInterferon-betaKidney Tubules, ProximalToll-Like Receptor 3Adaptor Proteins, Signal TransducingCells, CulturedGene Expression RegulationHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsPoly I-CRNA-Binding ProteinsSignal TransductionAdaptor Proteins, Signal TransducingChemokine CXCL10CXCL10 protein, humanIFIT1 protein, humanIFIT3 protein, humanInterferon-betaIntracellular Signaling Peptides and ProteinsPoly I-CRNA-Binding ProteinsTLR3 protein, humanToll-Like Receptor 3C‐X‐C motif chemokine ligand 10human renal proximal tubular epithelial cellinterferon‐stimulated gene 56interferon‐βToll‐like receptor 3

Identifiers

PMID38923445
PMCPMC11301256

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.