Evidence map›Paper›PMID 28009352›Full record

ArticleCell death and differentiation2017

A negative feedback loop of ICER and NF-κB regulates TLR signaling in innate immune responses.

Sihan Lv, Jian Li, Xinchen Qiu, Weida Li, Chao Zhang, Zhen-Ning Zhang, Bing Luan

Abstract read
In one paragraph

Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Article
  2. Review
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  7. Review
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  11. Ethanol Extract ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Common innate pathways to autoimmune disease.Clinical immunology (Orlando, Fla.) · 2020
    Review
  17. Article
  18. Article
  19. 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

7 authors.

Sihan LvDepartment of Endocrinology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Jian LiDepartment of Endocrinology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Xinchen QiuDepartment of Endocrinology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Weida LiTranslational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Chao ZhangTranslational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Zhen-Ning ZhangTranslational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Bing LuanDepartment of Endocrinology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NF-κB pathway has important roles in innate immune responses and its regulation is critical to maintain immune homeostasis. Here, we report a newly discovered feedback mechanism for the regulation of this pathway by TLR ligands in macrophages. Lipopolysaccharide (LPS) induced the expression of ICER via p38-mediated activation of CREB in macrophages. ICER, in turn, inhibited the transcriptional activity of NF-κB by direct interaction with the p65 subunit of NF-κB. Deficiency in ICER elevated binding of NF-κB to promoters of pro-inflammatory genes and their subsequent gene expression. Mice deficient in ICER were hypersensitive to LPS-induced endotoxic shock and showed propagated inflammation. Whereas ICER expression in ICER KO bone marrow transplanted mice rescued the ultra-inflammation phenotype, expression of a p65 binding-deficient ICER mutant failed to do so. Our results thus establish p38-CREB-ICER as key components of a negative feedback mechanism necessary to regulate TLR-driven inflammation.

Indexed as

Immunity, InnateAnimalsBone Marrow TransplantationCells, CulturedCyclic AMP Response Element ModulatorInflammationInterleukin-6LipopolysaccharidesLiverMacrophages, PeritonealMaleMiceMice, Inbred C57BLNF-kappa Bp38 Mitogen-Activated Protein KinasesPromoter Regions, GeneticCrem protein, mouseCyclic AMP Response Element ModulatorInterleukin-6LipopolysaccharidesNF-kappa Bp38 Mitogen-Activated Protein KinasesToll-Like ReceptorsTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID28009352
PMCPMC5344209

What OpenQuestion holds

Textmetadata
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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.