Evidence map›Paper›PMID 33089489›Full record

ArticleClinical and experimental immunology2021

Lipid antigens in bile from patients with chronic liver diseases activate natural killer T cells.

L Valestrand, N L Berntsen, F Zheng, E Schrumpf, S H Hansen, T H Karlsen, R S Blumberg, J R Hov, X Jiang, E Melum

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. The microbiota and the gut-liver axis in primary sclerosing cholangitis.Nature reviews. Gastroenterology & hepatology · 2023
    Review
  4. Article
  5. Article
  6. [Immune pathogenesis of primary biliary cholangitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
    Article
  7. 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

10 authors at 2 institutions in 2 countries.

L ValestrandNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.ORCID 0000-0001-9606-6837
N L BerntsenNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
F ZhengNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
E SchrumpfNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
S H HansenNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
T H KarlsenNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
R S BlumbergDivision of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
J R HovNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
X JiangNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
E MelumNorwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Oslo University Hospital · NOBrigham and Women's Hospital · US

Funding

Regulation of Mucosal LymphocytesR01DK051362 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg, Yu-Hwa Huang Blumberg · 1997 to 2026
$13.5M
INTESTINAL TRANSCYTOSIS OF IGG IN ADULT LIFER01DK053056 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BLUMBERG, RICHARD S · 1997 to 2021
$10.6M
MOLECULAR CHARACTERIZATION OF MUCOSAL LYMPHOCYTESR01DK044319 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg · 1992 to 2026
$10.4M
Endoplasmic reticulum stress and intestinal inflammationR01DK088199 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg · 2010 to 2026
$9.6M
NIDDK NIH HHS R01 DK044319NIDDK NIH HHS R01 DK051362NIDDK NIH HHS R01 DK053056NIDDK NIH HHS R01 DK088199
6 · The paper itself

Abstract

Natural killer T (NKT) cells are an abundant subset of liver lymphocytes activated by lipid antigens presented on CD1d molecules that are expressed by cholangiocytes. We aimed to determine if bile from patients with chronic liver diseases contains antigenic lipids that can activate NKT cells. Using murine invariant (24.7, 24.8 and DN32.D3) and non-invariant (14S.6, 14S.7 and 14S.10) NKT hybridomas we investigated the presence of lipid antigens in bile collected from the gallbladder of patients undergoing liver transplantation due to end-stage liver disease. Biliary microbiota profiles were generated using 16S rRNA amplicon sequencing. We found that the patient bile samples contain antigens that activate both invariant and non-invariant NKT hybridomas (24.7, 24.8, DN32.D3, 14S.6, 14S.7 and 14S.10), as demonstrated by activation of at least one hybridoma by eight of 10 bile samples. Activation at high dilutions suggests that some antigens are highly potent. We used the non-invariant NKT hybridoma 14S.6 to screen 21 additional patient bile samples for NKT-reactivity and demonstrated that 12 of 21 bile samples resulted in activation, three of which gave a strong activation. Four of 12 activating bile samples contained microbial DNA. Our results reveal an immunological pathway that could be of critical importance in biliary immunology.

Indexed as

AnimalsAntigensAntigens, CD1dBileCell LineHumansKiller Cells, NaturalLipidsLiverLiver DiseasesLymphocyte ActivationMiceNatural Killer T-CellsRNA, Ribosomal, 16SAntigensAntigens, CD1dLipidsRNA, Ribosomal, 16Sbiliary microbiotaCD1dcholangiocytePBCPSC

Identifiers

PMID33089489
PMCPMC7806449
OpenAlexW3094068856

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.