Evidence map›Paper›PMID 22989874›Full record

ArticleThe Journal of biological chemistry2012

CD3-T cell receptor co-stimulation through SLAMF3 and SLAMF6 receptors enhances RORγt recruitment to the IL17A promoter in human T lymphocytes.

Madhumouli Chatterjee, Christian M Hedrich, Thomas Rauen, Christina Ioannidis, Cox Terhorst, George C Tsokos

Open access · hybridAbstract read
In one paragraph

Article 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Human LY9 governs CD4Science immunology · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. [A preliminary study on SLAMF6 expression in patients with severe aplastic anemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2018
    Article
  10. SLE-Associated Defects Promote Altered T Cell Function.Critical reviews in immunology · 2017
    Review
  11. B cell-intrinsic CD84 and Ly108 maintain germinal center B cell tolerance.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Gene-function studies in systemic lupus erythematosus.Nature reviews. Rheumatology · 2013
    Review
  16. 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

6 authors at 2 institutions in 1 country.

Madhumouli ChatterjeeDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess MedicalCenter, Harvard Medical School, Boston, Massachusetts 02215, USA.
Christian M Hedrich
Thomas Rauen
Christina Ioannidis
Cox Terhorst
George C Tsokos
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
The Slamf3, Slamf5, and Slamf6 receptor-induced pathways to murine lupusP01AI065687 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TERHORST, CORNELIS P · 2006 to 2016
$14.7M
Gene Transcription In SLER01AI049954 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI George C Tsokos · 2002 to 2026
$5.8M
NIAID NIH HHS P01 AI065687NIAID NIH HHS R01 AI049954NIAID NIH HHS R01 AI49954 ANIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

Th17 lymphocytes play a key role during immune responses against bacteria and fungi and are involved in the pathophysiology of multiple autoimmune disorders. The co-stimulatory molecules SLAMF3 and SLAMF6 have been implicated in the formation of Th17 phenotypes and IL-17A expression. Increased surface expression of SLAMF3 and SLAMF6 has been linked with disease activity in systemic lupus erythematosus. Here we demonstrate that in human total T lymphocytes the canonical CD28 and the non-canonical SLAMF3/SLAMF6 co-stimulatory pathways cooperate in the recruitment of the transcription factor NFAT1 to the IL17A promoter. Furthermore, the dominance of the SLAMF3/SLAMF6 pathway in inducing IL-17A production can be attributed to an increased nuclear abundance and recruitment of RORγt to the IL17A promoter. Thus, we have identified an additional mechanism that may be central for the specific control of IL17A gene regulation in systemic lupus erythematosus T lymphocytes.

Indexed as

AntibodiesAntigens, CDCD28 AntigensCells, CulturedChromatin ImmunoprecipitationGene Expression RegulationGene Knockdown TechniquesHumansImmunoblottingInterleukin-17Lupus Erythematosus, SystemicMutationNFATC Transcription FactorsNuclear Receptor Subfamily 1, Group F, Member 3Promoter Regions, GeneticProtein BindingAntibodiesAntigens, CDCD28 AntigensInterleukin-17LY9 protein, humanNFATC2 protein, humanNFATC Transcription FactorsNuclear Receptor Subfamily 1, Group F, Member 3Receptor-CD3 Complex, Antigen, T-CellReceptors, Cell SurfaceSignaling Lymphocytic Activation Molecule FamilySignaling Lymphocytic Activation Molecule Family Member 1SLAMF6 protein, human

Identifiers

PMID22989874
PMCPMC3488086
OpenAlexW2014844398

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.