Evidence map›Paper›PMID 19166933›Full record

ArticleCellular signalling2009

Interleukin-1 regulates keratinocyte expression of T cell targeting chemokines through interleukin-1 receptor associated kinase-1 (IRAK1) dependent and independent pathways.

Julio C Sanmiguel, Florina Olaru, Jieliang Li, Elisabeth Mohr, Liselotte E Jensen

Abstract read
In one paragraph

Article in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Dermal αSMAThe EMBO journal · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Targeting the IL-1 family members in skin inflammation.Current opinion in investigational drugs (London, England : 2000) · 2010
    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

5 authors at 1 institution in 1 country.

Julio C SanmiguelDepartment of Pharmacology, University of Pennsylvania School of Medicine, 89 John Morgan Building, 3620 Hamilton Walk, Philadelphia, PA 19104, USA.
Florina Olaru
Jieliang Li
Elisabeth Mohr
Liselotte E Jensen
University of Pennsylvania · US

Funding

Soluble IL-1RAcP proteins as inhibitors of inflammationR03AR053672 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI JENSEN, LISELOTTE E · 2007 to 2009
$232k
NIAMS NIH HHS AR053672NIAMS NIH HHS R03 AR053672
6 · The paper itself

Abstract

IL-1 is a potent pro-inflammatory cytokine that activates intracellular signaling cascades some of which may involve IL-1 receptor associated kinase-1 (IRAK1). Psoriasis is a T cell dependent chronic inflammatory condition of the skin of unknown cause. IL-1 has been implicated in psoriasis pathology, but the mechanism has not been elucidated. Interestingly, expression of IRAK1 is elevated in psoriatic skin. To identify a potential link between IL-1, keratinocytes and T cells in skin inflammation we employed pathway-focused microarrays to evaluate IL-1 dependent gene expression in keratinocytes. Several candidate mRNAs encoding known T cell chemoattractants were identified in primary keratinocytes and the stable keratinocyte cell line HaCaT. CCL5 and CCL20 mRNA and protein levels were confirmed up-regulated by IL-1 in concentration and time-dependent manners. Furthermore IL-1 synergized with IFN-gamma and TNF-alpha. Expression of CXCL9, CXCL10 and CXCL11 mRNAs was also increased in response to IL-1, but protein could only be detected in medium from cells treated with IFN-gamma alone or in combination with IL-1. Over-expression of IRAK1 led to increased constitutive and cytokine induced production of CCL5 and CCL20. Inhibition of IRAK1 activity through RNAi or expression of a dominant negative mutant blocked production of CCL5 and CCL20 but had no effect upon the IL-1 enhancement of IFN-gamma induced CXCL9, CXCL10 and CXCL11 production. In conclusion IL-1 regulates T cell targeting chemokine production in keratinocytes through IRAK1 dependent and independent pathways. These pathways may contribute to acute and chronic skin inflammation.

Indexed as

Cell LineChemokines, CCChemokines, CXCHumansInterferon-gammaInterleukin-1Interleukin-1 Receptor-Associated KinasesKeratinocytesPsoriasisRNA InterferenceSignal TransductionT-LymphocytesTumor Necrosis Factor-alphaUp-RegulationChemokines, CCChemokines, CXCInterferon-gammaInterleukin-1Interleukin-1 Receptor-Associated KinasesTumor Necrosis Factor-alpha

Identifiers

PMID19166933
PMCPMC2650000
OpenAlexW2074163446

What OpenQuestion holds

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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.