Evidence map›Paper›PMID 21975862›Full record

ArticleKidney international2012

Interleukin-1 accounts for intrarenal Th17 cell activation during ureteral obstruction.

Jana Pindjakova, Shirley A Hanley, Michelle M Duffy, Caroline E Sutton, Gudrun A Weidhofer, Melinda N Miller, Karl A Nath, Kingston H G Mills, Rhodri Ceredig, Matthew D Griffin

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  10. Article
  11. Role of T cells in ischemic acute kidney injury and repair.The Korean journal of internal medicine · 2022
    Review
  12. IL-1 receptor signaling in podocytes limits susceptibility to glomerular damage.American journal of physiology. Renal physiology · 2022
    Article
  13. Article
  14. Article
  15. Review
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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 2 countries.

Jana PindjakovaRegenerative Medicine Institute, National Centre for Biomedical Engineering Science and School of Medicine, Nursing and Health Sciences, National University of Ireland, Galway, Ireland.
Shirley A Hanley
Michelle M Duffy
Caroline E Sutton
Gudrun A Weidhofer
Melinda N Miller
Karl A Nath
Kingston H G Mills
Rhodri Ceredig
Matthew D Griffin
Ollscoil na Gaillimhe – University of Galway · IEMayo Clinic · USTrinity College Dublin · IE

Funding

The Role of Dendritic Cells in Renal Immune ResponsesR01DK068545 · NIDDK · MAYO CLINIC ROCHESTER · PI NATH, KARL A. · 2004 to 2007
$1.3M
NIDDK NIH HHS DK68545NIDDK NIH HHS R01 DK068545
6 · The paper itself

Abstract

Interleukin 17A-secreting T-helper 17 (Th17) cells are pathogenic in inflammatory kidney diseases, but their intrarenal regulation is poorly understood. In order to better define Th17 cell dynamics during interstitial inflammation, we utilized the mouse unilateral ureteral obstruction model to analyze inflammatory cell subtypes by multicolor flow cytometry and cell sorting and by effects on in vitro-generated Th17 cells. Interleukin 17A expression localized to CCR6(+)CCR4(+/-)CD4(+) T-cells and progressively increased in obstructed kidneys. The number of CCR6(+)CD4(+) T-cells increased over 10-fold by 72 h, were enriched for interleukin 17A production, and were highly proliferative based on in vivo bromodeoxyuridine incorporation. Secreted products of leukocytes isolated from obstructed kidneys enhanced the interleukin 17A production of in vitro-generated Th17 cells. This Th17-enhancing activity was identified as interleukin-1 produced by renal dendritic cells and monocytes. The in vivo validity of these findings was confirmed in mice lacking the interleulin-1 receptor and in mice treated with a recombinant interleukin-1 receptor antagonist, each of which exhibited reduced intrarenal Th17 activity compared with control mice. Thus, the inflamed kidney accumulates CCR6(+) Th17 cells that undergo activation and proliferation. Production of interleukin 1 family cytokines by resident dendritic cells and infiltrating monocytes enhances intrarenal Th17 activation in acute kidney injury.

Indexed as

AnimalsCD4 AntigensCell ProliferationCells, CulturedDendritic CellsDisease Models, AnimalFemaleFlow CytometryInterleukin-1Interleukin-17Lymphocyte CountMiceMice, Inbred C57BLMonocytesNephritisReceptors, CCR4Ccr4 protein, mouseCCR6 protein, mouseCD4 AntigensInterleukin-1Interleukin-17Receptors, CCR4Receptors, CCR6

Identifiers

PMID21975862
PMCPMC3913378
OpenAlexW2065515194

What OpenQuestion holds

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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.