Evidence map›Paper›PMID 10190904›Full record

ArticleThe Journal of experimental medicine1999

Defective interleukin (IL)-18-mediated natural killer and T helper cell type 1 responses in IL-1 receptor-associated kinase (IRAK)-deficient mice.

P Kanakaraj, K Ngo, Y Wu, A Angulo, P Ghazal, C A Harris, J J Siekierka, P A Peterson, W P Fung-Leung

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 159 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Interleukin-18 in Health and Disease.International journal of molecular sciences · 2019
    Review
  11. Article
  12. Article
  13. The pathological role of IL-18Rα in renal ischemia/reperfusion injury.Laboratory investigation; a journal of technical methods and pathology · 2015
    Article
  14. Article
  15. Review
  16. IL-18 in inflammatory and autoimmune disease.Cellular and molecular life sciences : CMLS · 2013
    Review
  17. Article
  18. Article
  19. Article
  20. 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 at 1 institution in 1 country.

P KanakarajR.W. Johnson Pharmaceutical Research Institute, San Diego, California 92121, USA.
K Ngo
Y Wu
A Angulo
P Ghazal
C A Harris
J J Siekierka
P A Peterson
W P Fung-Leung
Scripps Research Institute · US

Funding

TRANSCRIPTION FACTORS AND HUMAN CMV PATHOGENESISR01AI030627 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI GHAZAL, PETER · 1997 to 1999
–
ROLE OF RETINOIDS IN HUMAN CYTOMEGALOVIRUS LATENCYR01CA066167 · NCI · SCRIPPS RESEARCH INSTITUTE · PI GHAZAL, PETER · 1994 to 1997
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TRANSCRIPTION FACTORS AND HUMAN CMV PATHOGENESISR29AI030627 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI GHAZAL, PETER · 1992 to 1996
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NCI NIH HHS CA66167NIAID NIH HHS AI30627
6 · The paper itself

Abstract

Interleukin (IL)-18 is functionally similar to IL-12 in mediating T helper cell type 1 (Th1) response and natural killer (NK) cell activity but is related to IL-1 in protein structure and signaling, including recruitment of IL-1 receptor-associated kinase (IRAK) to the receptor and activation of c-Jun NH2-terminal kinase (JNK) and nuclear factor (NF)-kappaB. The role of IRAK in IL-18-induced responses was studied in IRAK-deficient mice. Significant defects in JNK induction and partial impairment in NF-kappaB activation were found in IRAK-deficient Th1 cells, resulting in a dramatic decrease in interferon (IFN)-gamma mRNA expression. In vivo Th1 response to Propionibacterium acnes and lipopolysaccharide in IFN-gamma production and induction of NK cytotoxicity by IL-18 were severely impaired in IRAK-deficient mice. IFN-gamma production by activated NK cells in an acute murine cytomegalovirus infection was significantly reduced despite normal induction of NK cytotoxicity. These results demonstrate that IRAK plays an important role in IL-18-induced signaling and function.

Indexed as

Mitogen-Activated Protein KinasesAnimalsCalcium-Calmodulin-Dependent Protein KinasesCell DifferentiationCell DivisionChimeraCrosses, GeneticCytomegalovirus InfectionsCytotoxicity, ImmunologicDepression, ChemicalEnzyme ActivationEnzyme InductionFemaleGene Expression RegulationInterferon-gammaInterleukin-18Calcium-Calmodulin-Dependent Protein KinasesIl18r1 protein, mouseInterferon-gammaInterleukin-18Interleukin-18 Receptor alpha SubunitInterleukin-1 Receptor-Associated KinasesInterleukin-4JNK Mitogen-Activated Protein KinasesLipopolysaccharidesMitogen-Activated Protein KinasesNF-kappa BProtein KinasesReceptors, InterleukinReceptors, Interleukin-18

Identifiers

PMID10190904
PMCPMC2193007
OpenAlexW2143774231

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.