Evidence map›Paper›PMID 27851911›Full record

ArticleImmunity2016

Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney.

Christian F Krebs, Hans-Joachim Paust, Sonja Krohn, Tobias Koyro, Silke R Brix, Jan-Hendrik Riedel, Patricia Bartsch, Thorsten Wiech, Catherine Meyer-Schwesinger, Jiabin Huang and 14 more

Open access · hybridAbstract read
In one paragraph

Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

114 citing papers in PubMed, 197 citations in OpenAlex.

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  13. Mitigation of Ferroptosis in Diabetic Kidney Disease Through Mesenchymal Stem Cell Intervention via the Smad2/3/METTL3/S1PR1 Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. The immune mechanisms of the urinary tract against infections.Frontiers in cellular and infection microbiology · 2025
    Review
  19. Review
  20. Article

54 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 4 institutions in 2 countries.

Christian F KrebsIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Hans-Joachim PaustIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Sonja KrohnIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Tobias KoyroIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Silke R BrixIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Jan-Hendrik RiedelIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Patricia BartschIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Thorsten WiechInstitut für Pathologie, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Catherine Meyer-SchwesingerIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Jiabin HuangInstitut für Medizinische Mikrobiologie, Virologie, und Hygiene, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Nicole FischerInstitut für Medizinische Mikrobiologie, Virologie, und Hygiene, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Philipp BuschKlinik für Allgemeinchirurgie, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Hans-Willi MittrückerInstitut für Immunologie, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Ulrich SteinhoffPhilipps-Universität Marburg, Institut für Medizinische Mikrobiologie und Krankenhaushygiene, 35043 Marburg, Germany.
Brigitta StockingerThe Francis Crick Institute, Midland Road, London NW1 1AT, UK.
Laura Garcia PerezI. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Ulrich O WenzelIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Matthias JanneckIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Oliver M SteinmetzIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Nicola GaglianiKlinik für Allgemeinchirurgie, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Rolf A K StahlIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Samuel HuberI. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Jan-Eric TurnerIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany.
Ulf PanzerIII. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, 20251 Hamburg, Germany. Electronic address: panzer@uke.de.
Universität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEPhilipps University of Marburg · DEThe Francis Crick Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Th17 cells are most abundant in the gut, where their presence depends on the intestinal microbiota. Here, we examined whether intestinal Th17 cells contribute to extra-intestinal Th17 responses in autoimmune kidney disease. We found high frequencies of Th17 cells in the kidneys of patients with antineutrophil cytoplasmatic antibody (ANCA)-associated glomerulonephritis. We utilized photoconversion of intestinal cells in Kaede mice to track intestinal T cell mobilization upon glomerulonephritis induction, and we found that Th17 cells egress from the gut in a S1P-receptor-1-dependent fashion and subsequently migrate to the kidney via the CCL20/CCR6 axis. Depletion of intestinal Th17 cells in germ-free and antibiotic-treated mice ameliorated renal disease, whereas expansion of these cells upon Citrobacter rodentium infection exacerbated pathology. Thus, in some autoimmune settings, intestinal Th17 cells migrate into target organs, where they contribute to pathology. Targeting the intestinal Th17 cell "reservoir" may present a therapeutic strategy for these autoimmune disorders.

Indexed as

AnimalsAutoimmune DiseasesChemotaxis, LeukocyteCitrobacter rodentiumDisease Models, AnimalEnterobacteriaceae InfectionsFlow CytometryGlomerulonephritisHumansIntestinesKidneyMiceMice, Inbred C57BLMice, TransgenicReal-Time Polymerase Chain ReactionReceptors, LysosphingolipidReceptors, LysosphingolipidS1PR1 protein, humanS1pr1 protein, mouseSphingosine-1-Phosphate Receptors

Identifiers

PMID27851911
PMCPMC6381450
OpenAlexW2552808209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.