Evidence map›Paper›PMID 27169420›Full record

ReviewPediatric nephrology (Berlin, Germany)2017

Innate and adaptive immunity in experimental glomerulonephritis: a pathfinder tale.

Katharina Artinger, Alexander H Kirsch, Ida Aringer, Foteini Moschovaki-Filippidou, Philipp Eller, Alexander R Rosenkranz, Kathrin Eller

Open access · hybridAbstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. IL-17C/IL-17 Receptor E Signaling in CD4Journal of the American Society of Nephrology : JASN · 2018
    Article
  13. CTGF in kidney fibrosis and glomerulonephritis.Inflammation and regeneration · 2018
    Review
  14. Specialized Regulatory T Cells for Optimal Suppression of T Cell Responses in GN.Journal of the American Society of Nephrology : JASN · 2017
    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

7 authors at 1 institution in 1 country.

Katharina ArtingerClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria.
Alexander H KirschClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria.
Ida AringerClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria.
Foteini Moschovaki-FilippidouClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria.
Philipp EllerIntensive Care Unit, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Alexander R RosenkranzClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria.
Kathrin EllerClinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria. kathrin.eller@medunigraz.at.
Medical University of Graz · AT

Funding

Austrian Science Fund (FWF) P-21402Austrian Science Fund (FWF) P-27537Austrian Science Fund (FWF) W1241
6 · The paper itself

Abstract

The role of innate and adaptive immune cells in the experimental model of nephrotoxic serum nephritis (NTS) has been rigorously studied in recent years. The model is dependent on kidney-infiltrating T helper (TH) 17 and TH1 cells, which recruit neutrophils and macrophages, respectively, and cause sustained kidney inflammation. In a later phase of disease, regulatory T cells (Tregs) infiltrate the kidney in an attempt to limit disease activity. In the early stage of NTS, lymph node drainage plays an important role in disease initiation since dendritic cells present the antigen to T cells in the T cell zones of the draining lymph nodes. This results in the differentiation and proliferation of TH17 and TH1 cells. In this setting, immune regulatory cells (Tregs), namely, CCR7-expressing Tregs and mast cells (MCs), which are recruited by Tregs via the production of interleukin-9, exert their immunosuppressive capacity. Together, these two cell populations inhibit T cell differentiation and proliferation, thereby limiting disease activity by as yet unknown mechanisms. In contrast, the spleen plays no role in immune activation in NTS, but constitutes a place of extramedullary haematopoiesis. The complex interactions of immune cells in NTS are still under investigation and might ultimately lead to targeted therapies in glomerulonephritis.

Indexed as

Adaptive ImmunityImmunity, InnateAnimalsCell DifferentiationCell ProliferationDisease Models, AnimalGlomerulonephritisHumansInterleukin-9KidneyLymph NodesMast CellsMiceReceptors, CCR7SpleenTh17 CellsCcr7 protein, mouseInterleukin-9Receptors, CCR7ChemokinesImmune systemLymph nodeNephrotoxic serum nephritisRegulatory T-cellT cell

Identifiers

PMID27169420
PMCPMC5399043
OpenAlexW2349130333

What OpenQuestion holds

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LicenceCC BY
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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.