Evidence map›Paper›PMID 34054816›Full record

ArticleFrontiers in immunology2021

DDX3X Links NLRP11 to the Regulation of Type I Interferon Responses and NLRP3 Inflammasome Activation.

Ioannis Kienes, Sarah Bauer, Clarissa Gottschild, Nora Mirza, Jens Pfannstiel, Martina Schröder, Thomas A Kufer

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. 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
2.0field-weighted citation impact, top 13% of its field
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, 36 citations in OpenAlex.

  1. Review
  2. An overview of human inflammasomes: Activation and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023
    Review
  13. Article
  14. NOD-like Receptors-Emerging Links to Obesity and Associated Morbidities.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. The human DEAD-box helicase DDX3X as a regulator of mRNA translation.Frontiers in cell and developmental biology · 2022
    Review
  19. A Dual Role of DDX3X in dsRNA-Derived Innate Immune Signaling.Frontiers in molecular biosciences · 2022
    Review
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 at 2 institutions in 2 countries.

Ioannis KienesDepartment of Immunology, Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
Sarah BauerDepartment of Immunology, Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
Clarissa GottschildDepartment of Immunology, Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
Nora MirzaDepartment of Immunology, Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
Jens PfannstielCore Facility University of Hohenheim, Mass Spectrometry Module, University of Hohenheim, Stuttgart, Germany.
Martina SchröderKathleen Lonsdale Institute for Human Health Research, Department of Biology, Maynooth University, Maynooth, Ireland.
Thomas A KuferDepartment of Immunology, Institute of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
University of Hohenheim · DENational University of Ireland, Maynooth · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tight regulation of inflammatory cytokine and interferon (IFN) production in innate immunity is pivotal for optimal control of pathogens and avoidance of immunopathology. The human Nod-like receptor (NLR) NLRP11 has been shown to regulate type I IFN and pro-inflammatory cytokine responses. Here, we identified the ATP-dependent RNA helicase DDX3X as a novel binding partner of NLRP11, using co-immunoprecipitation and LC-MS/MS. DDX3X is known to enhance type I IFN responses and NLRP3 inflammasome activation. We demonstrate that NLRP11 can abolish IKKϵ-mediated phosphorylation of DDX3X, resulting in lower type I IFN induction upon viral infection. These effects were dependent on the LRR domain of NLRP11 that we mapped as the interaction domain for DDX3X. In addition, NLRP11 also suppressed NLRP3-mediated caspase-1 activation in an LRR domain-dependent manner, suggesting that NLRP11 might sequester DDX3X and prevent it from promoting NLRP3-induced inflammasome activation. Taken together, our data revealed DDX3X as a central target of NLRP11, which can mediate the effects of NLRP11 on type I IFN induction as well as NLRP3 inflammasome activation. This expands our knowledge of the molecular mechanisms underlying NLRP11 function in innate immunity and suggests that both NLRP11 and DDX3X might be promising targets for modulation of innate immune responses.

Indexed as

Chromatography, LiquidCytokinesDEAD-box RNA HelicasesHumansImmunity, InnateInflammasomesInflammation MediatorsInterferon Type INLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsProtein BindingTandem Mass SpectrometryCytokinesDDX3X protein, humanDEAD-box RNA HelicasesInflammasomesInflammation MediatorsInterferon Type INLR Family, Pyrin Domain-Containing 3 ProteinNLRP11 protein, humanNLR Proteinsanti-viralDEAD-box helicaseIL-1inflammasomeinnate immunitynod-like receptorstype I interferon

Identifiers

PMID34054816
PMCPMC8158815
OpenAlexW3160755074

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.