Evidence map›Paper›PMID 29993279›Full record

ArticleAmerican journal of physiology. Renal physiology2018

Activated natural killer T cells in mice induce acute kidney injury with hematuria through possibly common mechanisms shared by human CD56

Takahiro Uchida, Hiroyuki Nakashima, Seigo Ito, Takuya Ishikiriyama, Masahiro Nakashima, Shuhji Seki, Hiroo Kumagai, Naoki Oshima

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Resident T Cells and Intrarenal Inflammation.Journal of the American Society of Nephrology : JASN · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Role of T cells in ischemic acute kidney injury and repair.The Korean journal of internal medicine · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury.International journal of molecular sciences · 2019
    Review
  17. 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

8 authors at 1 institution in 1 country.

Takahiro UchidaDepartment of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama , Japan.
Hiroyuki NakashimaDepartment of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Saitama , Japan.
Seigo ItoDepartment of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama , Japan.
Takuya IshikiriyamaDepartment of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Saitama , Japan.
Masahiro NakashimaDepartment of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Saitama , Japan.
Shuhji SekiDepartment of Immunology and Microbiology, National Defense Medical College, Tokorozawa, Saitama , Japan.
Hiroo KumagaiDepartment of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama , Japan.
Naoki OshimaDepartment of Nephrology and Endocrinology, National Defense Medical College, Tokorozawa, Saitama , Japan.
National Defense Medical College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although activation of mouse natural killer T (NKT) cells by α-galactosylceramide (α-GalCer) causes failure of multiple organs, including the kidneys, the precise mechanisms underlying kidney injury remain unclear. Here, we showed that α-GalCer-activated mouse NKT cells injured both kidney vascular endothelial cells and tubular epithelial cells in vitro, causing acute kidney injury (AKI) with hematuria in middle-aged mice. The perforin-mediated pathway was mainly involved in glomerular endothelial cell injury, whereas the TNF-α/Fas ligand pathway played an important role in the injury of tubular epithelial cells. Kidney injury in young mice was mild but could be significantly exacerbated if NKT cells were strongly activated by NK cell depletion alone or in combination with IL-12 pretreatment. When stimulated by a combination of IL-2 and IL-12, human CD56

Indexed as

Cytotoxicity, ImmunologicLymphocyte ActivationAcute Kidney InjuryAge FactorsAnimalsCD56 AntigenCell LineCoculture TechniquesEndothelial CellsEpithelial CellsFas Ligand ProteinFemaleGalactosylceramidesHematuriaHumansKidney Tubules, Proximalalpha-galactosylceramideCD56 AntigenFas Ligand ProteinFasl protein, mouseGalactosylceramidesNCAM1 protein, humanperforin, mousePore Forming Cytotoxic ProteinsTnf protein, mouseTumor Necrosis Factor-alphaacute kidney injuryCD56+ T cellFas ligandnatural killer T cellperforin

Identifiers

PMID29993279
PMCPMC6172573
OpenAlexW2867036078

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.