Evidence map›Paper›PMID 23138484›Full record

ArticleJournal of the American Society of Nephrology : JASN2012

Immature renal dendritic cells recruit regulatory CXCR6(+) invariant natural killer T cells to attenuate crescentic GN.

Jan-Hendrik Riedel, Hans-Joachim Paust, Jan-Eric Turner, André P Tittel, Christian Krebs, Erik Disteldorf, Claudia Wegscheid, Gisa Tiegs, Joachim Velden, Hans-Willi Mittrücker and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 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
2.6field-weighted citation impact, top 10% 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, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022
    Review
  6. Article
  7. Unconventional T cells and kidney disease.Nature reviews. Nephrology · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury.International journal of molecular sciences · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Tissue-Resident Lymphocytes in the Kidney.Journal of the American Society of Nephrology : JASN · 2018
    Review
  18. Opposing Roles of Dendritic Cell Subsets in Experimental GN.Journal of the American Society of Nephrology : JASN · 2018
    Article
  19. 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

15 authors at 2 institutions in 1 country.

Jan-Hendrik RiedelUniversitätsklinikum Hamburg-Eppendorf, III Medizinische Klinik, Martinistrasse 52, 20246 Hamburg, Germany.
Hans-Joachim Paust
Jan-Eric Turner
André P Tittel
Christian Krebs
Erik Disteldorf
Claudia Wegscheid
Gisa Tiegs
Joachim Velden
Hans-Willi Mittrücker
Natalio Garbi
Rolf A K Stahl
Oliver M Steinmetz
Christian Kurts
Ulf Panzer
Institut für Medizinische Informatik, Biometrie und Epidemiologie · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immature renal dendritic cells (DCs) are protective early in murine crescentic GN, but the mechanisms underlying this protection are unknown. Here, depletion of DCs reduced the recruitment of invariant natural killer T (iNKT) cells, which attenuate GN, into the kidney in the early stage of experimental crescentic GN. More than 90% of renal iNKT cells expressed the chemokine receptor CXCR6, and renal DCs produced high amounts of the cognate ligand CXCL16 early after induction of nephritis, suggesting that renal DC-derived CXCL16 might attract protective CXCR6(+) iNKT cells. Consistent with this finding, CXCR6-deficient mice exhibited less iNKT cell recruitment and developed nephritis that was more severe, similar to the aggravated nephritis observed in mice depleted of immature DCs. Finally, adoptive transfer of CXCR6-competent NKT cells ameliorated nephritis. Taken together, these results suggest an immunoprotective mechanism involving immature DCs, CXCL16, CXCR6, and regulatory iNKT cells, which might stimulate the development of new therapeutic strategies for GN.

Indexed as

AnimalsChemokine CXCL16Chemokine CXCL6Dendritic CellsGlomerulonephritisLeukocytes, MononuclearMaleMiceMice, Inbred C57BLReceptors, CXCRReceptors, CXCR6SheepChemokine CXCL16Chemokine CXCL6Cxcl16 protein, mouseCxcr6 protein, mouseReceptors, CXCRReceptors, CXCR6

Identifiers

PMID23138484
PMCPMC3507367
OpenAlexW2160581006

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.