Evidence map›Paper›PMID 28295231›Full record

ArticleEuropean journal of immunology2017

Deficiency in IRAK4 activity attenuates manifestations of murine Lupus.

Michael Murphy, Goutham Pattabiraman, Tissa T Manavalan, Andrei E Medvedev

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Targeting the Myddosome in Systemic Autoimmunity: Ready for Prime Time?Arthritis & rheumatology (Hoboken, N.J.) · 2021
    Article
  8. Kinase inhibition in autoimmunity and inflammation.Nature reviews. Drug discovery · 2021
    Review
  9. Article
  10. Article
  11. 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

4 authors at 1 institution in 1 country.

Michael MurphyDepartment of Immunology, University of Connecticut Health Center, Farmington, CT, USA.
Goutham PattabiramanDepartment of Immunology, University of Connecticut Health Center, Farmington, CT, USA.
Tissa T ManavalanDepartment of Immunology, University of Connecticut Health Center, Farmington, CT, USA.
Andrei E MedvedevDepartment of Immunology, University of Connecticut Health Center, Farmington, CT, USA.
UConn Health · US

Funding

IRAK4 and systemic lupus erythematosusR21AI099430 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MEDVEDEV, ANDREI E · 2013 to 2014
$425k
NIAID NIH HHS R21 AI099430
6 · The paper itself

Abstract

Interleukin-1 receptor-associated kinase (IRAK) 4 mediates host defense against infections. As an active kinase, IRAK4 elicits full spectra of myeloid differentiation primary response protein (MyD) 88-dependent responses, while kinase-inactive IRAK4 induces a subset of cytokines and negative regulators whose expression is not regulated by mRNA stability. IRAK4 kinase activity is critical for resistance against Streptococcus pneumoniae, but its involvement in autoimmunity is incompletely understood. In this study, we determined the role of IRAK4 kinase activity in murine lupus. Lupus development in BXSB mice expressing the Y chromosome autoimmunity accelerator (Yaa) increased basal and Toll-like receptor (TLR) 4/7-induced phosphorylation of mitogen-activated protein kinases, p65 nuclear factor-κB (NF-κB), enhanced tumor necrosis factor (TNF)-α and C-C motif chemokine ligand (CCL) 5 gene expression in splenic macrophages, but decreased levels of Toll-interacting protein and IRAK-M, without affecting IRAK4 or IRAK1 expression. Mice harboring kinase-inactive IRAK4 on the lupus-prone Yaa background manifested blunted TLR signaling in macrophages and reduced glomerulonephritis, splenomegaly, serum anti-nuclear antibodies, numbers of splenic macrophages, total and TNF-α

Indexed as

AutoimmunityImmunologic Deficiency SyndromesAnimalsChemokine CCL5CytokinesInterleukin-1 Receptor-Associated KinasesLupus NephritisMacrophagesMiceMitogen-Activated Protein KinasesNF-kappa BPhosphorylationPrimary Immunodeficiency DiseasesSignal TransductionSpleenToll-Like ReceptorsCcl5 protein, mouseChemokine CCL5CytokinesInterleukin-1 Receptor-Associated KinasesIrak4 protein, mouseMitogen-Activated Protein KinasesNF-kappa BToll-Like ReceptorsTumor Necrosis Factor-alphaAutoimmunityInnate ImmunityIRAK4Macrophage Toll-like receptors (TLRs)

Identifiers

PMID28295231
PMCPMC5575829
OpenAlexW2591994964

What OpenQuestion holds

Textmetadata
LicenceTDM
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.