Evidence map›Paper›PMID 22184122›Full record

Trial reportThe Journal of biological chemistry2012

cAMP-responsive element modulator α (CREMα) suppresses IL-17F protein expression in T lymphocytes from patients with systemic lupus erythematosus (SLE).

Christian M Hedrich, Thomas Rauen, Katalin Kis-Toth, Vasileios C Kyttaris, George C Tsokos

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. HLA-DRB1Frontiers in medicine · 2020
    Article
  15. Article
  16. Review
  17. [Effect of aberrant H3K27me3 modification in promoter regions on cAMP response element modulator α expression in CD4Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017
    Article
  18. Article
  19. Epigenetics in SLE.Current rheumatology reports · 2017
    Review
  20. 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

5 authors at 2 institutions in 2 countries.

Christian M HedrichDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA. chedrich@bidmc.harvard.edu
Thomas Rauen
Katalin Kis-Toth
Vasileios C Kyttaris
George C Tsokos
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Expanded Double Negative T cells in SLE.R01AI085567 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2010 to 2025
$6.8M
LYMPHOCYTE SIGNALING DEFECTS IN PATIENTS WITH LUPUSR01AI042269 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI TSOKOS, GEORGE C · 1998 to 2017
$6.8M
Gene Transcription In SLER01AI049954 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI George C Tsokos · 2002 to 2026
$5.8M
Gene transcription in SLER37AI049954 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2013 to 2022
$4.8M
The Role of Interleukin 23 in LupusR01AR060849 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KYTTARIS, VASILEIOS CHRISTOS · 2012 to 2016
$1.9M
NFAT/AP-1 cooperation in SLE T cellsK23AR055672 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KYTTARIS, VASILEIOS CHRISTOS · 2008 to 2012
$486k
NIAID NIH HHS R01 AI042269NIAID NIH HHS R01 AI049954NIAID NIH HHS R01 AI085567NIAID NIH HHS R01 AI42269NIAID NIH HHS R01 AI49954NIAID NIH HHS R01AI85567NIAID NIH HHS R37 AI049954NIAMS NIH HHS K23 AR055672NIAMS NIH HHS R01 AR060849
6 · The paper itself

Abstract

The proinflammatory cytokines IL-17A and IL-17F are primarily produced by Th17 lymphocytes. Both are involved in host defense mechanisms against bacterial and fungal pathogens and contribute to the development of various autoimmune diseases. T lymphocytes from patients with systemic lupus erythematosus (SLE) display increased expression of transcription factor cAMP-responsive element modulator α (CREMα), which has been documented to account for aberrant T cell function and contributes to the pathogenesis of SLE. Here, we provide evidence that IL-17F expression is reduced in SLE T cells. We demonstrate that CREMα binds to a yet unidentified CRE site within the proximal promoter. This results in reduced IL-17F expression in SLE T lymphocytes and is independent of activating epigenetic patterns (increased histone H3 Lys-18 acetylation, reduced histone H3 Lys-27 trimethylation, and CpG-DNA demethylation). Forced CREMα expression in human T lymphocytes results in reduced IL-17F expression. Our findings demonstrate extended involvement of CREMα in cytokine dysregulation in SLE by contributing to a disrupted balance between IL-17A and IL-17F. An increased IL-17A/IL-17F ratio may aggravate the proinflammatory phenotype of SLE.

Indexed as

Epigenesis, GeneticResponse ElementsAcetylationAdultCpG IslandsCyclic AMP Response Element ModulatorFemaleHistonesHumansInterleukin-17Jurkat CellsLupus Erythematosus, SystemicMethylationMiddle AgedTh17 CellsCREM protein, humanCyclic AMP Response Element ModulatorHistonesIL17A protein, humanIL17F protein, humanInterleukin-17

Identifiers

PMID22184122
PMCPMC3281648
OpenAlexW2108673463

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.