Evidence map›Paper›PMID 19016912›Full record

ArticleImmunology2009

Modulation of nuclear factor-kappaB activity can influence the susceptibility to systemic lupus erythematosus.

Alexis M Kalergis, Mirentxu I Iruretagoyena, Magaly J Barrientos, Pablo A González, Andres A Herrada, Eduardo D Leiva, Miguel A Gutiérrez, Claudia A Riedel, Susan M Bueno, Sergio H Jacobelli

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Diterpenes: Nature's Hidden Gems of Immunomodulation.International journal of molecular sciences · 2025
    Review
  3. New insights into the Lck-NF-κB signaling pathway.Frontiers in cell and developmental biology · 2023
    Review
  4. Review
  5. Article
  6. Role of A20/TNFAIP3 deficiency in lupus nephritis in MRL/lpr mice.Clinical and experimental nephrology · 2020
    Article
  7. Potential Molecular Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Dendritic Cells and Macrophages: Sentinels in the Kidney.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Review
  17. Article
  18. Article
  19. Article
  20. ABIN1 dysfunction as a genetic basis for lupus nephritis.Journal of the American Society of Nephrology : JASN · 2013
    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

10 authors at 3 institutions in 1 country.

Alexis M KalergisMillennium Nucleus on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile. akalergis@bio.puc.cl/kalergis@vtr.net
Mirentxu I Iruretagoyena
Magaly J Barrientos
Pablo A González
Andres A Herrada
Eduardo D Leiva
Miguel A Gutiérrez
Claudia A Riedel
Susan M Bueno
Sergio H Jacobelli
Millennium Institute on Immunology and Immunotherapy · CLPontificia Universidad Católica de Chile · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune diseases, such as systemic lupus erythematosus (SLE), result from deficiencies in self-antigen tolerance processes, which require regulated dendritic cell (DC) function. In this study we evaluated the phenotype of DCs during the onset of SLE in a mouse model, in which deletion of the inhibitory receptor FcgammaRIIb leads to the production of anti-nuclear antibodies and glomerulonephritis. Splenic DCs from FcgammaRIIb-deficient mice suffering from SLE showed increased expression of co-stimulatory molecules. Furthermore, diseased mice showed an altered function of the nuclear factor-kappaB (NF-kappaB) transcription factor, which is involved in DC maturation. Compared with healthy animals, expression of the inhibitory molecule IkappaB-alpha was significantly decreased in mice suffering from SLE. Consistently, pharmacological inhibition of NF-kappaB activity in FcgammaRIIb-deficient mice led to reduced susceptibility to SLE and prevented symptoms, such as anti-nuclear antibodies and kidney damage. Our data suggest that the occurrence of SLE is significantly influenced by alterations of NF-kappaB function, which can be considered as a new therapeutic target for this disease.

Indexed as

AnimalsAnti-Inflammatory AgentsDendritic CellsDiterpenesFemaleGlomerulonephritisHypoglycemic AgentsI-kappa B ProteinsLupus Erythematosus, SystemicMiceMice, Inbred C57BLMice, KnockoutNF-kappa BReceptors, IgGRosiglitazoneThiazolidinedionesandrographolideAnti-Inflammatory AgentsDiterpenesFcgr2b protein, mouseHypoglycemic AgentsI-kappa B ProteinsNF-kappa BReceptors, IgGRosiglitazoneThiazolidinediones

Identifiers

PMID19016912
PMCPMC2753943
OpenAlexW2073027199

What OpenQuestion holds

Textmetadata
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.