Evidence map›Paper›PMID 20950612›Full record

ArticleGastroenterology2011

Sulfatide-mediated activation of type II natural killer T cells prevents hepatic ischemic reperfusion injury in mice.

Philomena Arrenberg, Igor Maricic, Vipin Kumar

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

73 citing papers in PubMed, 107 citations in OpenAlex.

  1. Review
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  8. Animal models for transplant immunology: bridging bench to bedside.Clinical transplantation and research · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. The role of natural killer T cells in liver transplantation.Frontiers in cell and developmental biology · 2023
    Review
  14. Review
  15. Review
  16. Immune response associated with ischemia and reperfusion injury during organ transplantation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Article

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

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

3 authors at 1 institution in 1 country.

Philomena ArrenbergLaboratory of Autoimmunity, Torrey Pines Institute for Molecular Studies, San Diego, California 92121, USA.
Igor Maricic
Vipin Kumar
Torrey Pines Institute For Molecular Studies · US

Funding

Sulfatide-reactive type II NKT cells: repertoire and functionR01CA100660 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KUMAR, VIPIN · 2004 to 2014
$3.5M
NCI NIH HHS R01 CA100660NCI NIH HHS R01-CA100660
6 · The paper itself

Abstract

BACKGROUND &

aimsHepatic ischemic reperfusion injury (IRI) is a major complication of liver transplantation and resectional hepatic surgeries. Natural killer T (NKT) cells predominate in liver, where they recognize lipid antigens bound to CD1d molecules. Type I NKT cells use a semi-invariant T-cell receptor and react with α-galactosylceramide; type II NKT cells use diverse T-cell receptors. Some type II NKT cells recognize the self-glycolipid sulfatide. It is not clear whether or how these distinct NKT cell subsets mediate hepatocellular damage after IRI.

methodsWe examined the roles of type I and type II NKT cells in mice with partial hepatic, warm ischemia, and reperfusion injury.

resultsMice that lack type I NKT cells (Jα18-/-) were protected from hepatic IRI, indicated by reduced hepatocellular necrosis and serum levels of alanine aminotransferase. Sulfatide-mediated activation of type II NKT cells reduced interferon-γ secretion by type I NKT cells and prevented IRI. Protection from hepatic IRI by sulfatide-mediated inactivation of type I NKT cells was associated with significant reductions in hepatic recruitment of myeloid cell subsets, especially the CD11b(+)Gr-1(int), Gr-1(-), and NK cells.

conclusionsIn mice, subsets of NKT cells have opposing roles in hepatic IRI: type I NKT cells promote injury whereas sulfatide-reactive type II NKT cells protect against injury. CD1d activation of NKT cells is conserved from mice to human beings, so strategies to modify these processes might be developed to treat patients with hepatic reperfusion injury.

Indexed as

AnimalsCD11b AntigenFemaleInterferon-gammaLiverMiceMice, Inbred C57BLMyeloid CellsNatural Killer T-CellsNecrosisReceptors, ChemokineReperfusion InjurySulfoglycosphingolipidsCD11b AntigenGr-1 protein, mouseInterferon-gammaReceptors, ChemokineSulfoglycosphingolipids

Identifiers

PMID20950612
PMCPMC3114423
OpenAlexW2141515779

What OpenQuestion holds

Textmetadata
LicenceTDM
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.