Evidence map›Paper›PMID 26755880›Full record

ReviewWorld journal of gastroenterology2016

Xenobiotics and loss of tolerance in primary biliary cholangitis.

Jinjun Wang, Guoxiang Yang, Alana Mari Dubrovsky, Jinjung Choi, Patrick S C Leung

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Dietary therapy of murine primary biliary cholangitis induces hepatocellular steatosis: A cautionary tale.Liver international : official journal of the International Association for the Study of the Liver · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. 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

5 authors at 1 institution in 2 countries.

Jinjun WangJinjun Wang, Guoxiang Yang, Alana Mari Dubrovsky, Jinjung Choi, Patrick SC Leung, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, CA 95616, United States.
Guoxiang YangJinjun Wang, Guoxiang Yang, Alana Mari Dubrovsky, Jinjung Choi, Patrick SC Leung, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, CA 95616, United States.
Alana Mari DubrovskyJinjun Wang, Guoxiang Yang, Alana Mari Dubrovsky, Jinjung Choi, Patrick SC Leung, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, CA 95616, United States.
Jinjung ChoiJinjun Wang, Guoxiang Yang, Alana Mari Dubrovsky, Jinjung Choi, Patrick SC Leung, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, CA 95616, United States.
Patrick S C LeungJinjun Wang, Guoxiang Yang, Alana Mari Dubrovsky, Jinjung Choi, Patrick SC Leung, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, CA 95616, United States.
Yangzhou University · CN

Funding

XENOBIOTICS AND PRIMARY BILIARY CIRRHOSISR01DK067003 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI GERSHWIN, MERRILL E · 2003 to 2017
$4.4M
dnTGF Beta RII Mice and PBCR01DK090019 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GERSHWIN, MERRILL E, RIDGWAY, WILLIAM M · 2010 to 2017
$3.8M
MECHANISMS AND PATHOGENESIS OF PRIMARY BILIARY CIRRHOSISR37DK039588 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI GERSHWIN, MERRILL E · 2001 to 2010
$3.5M
MECHANISMS AND PATHOGENESIS OF PRIMARY BILIARY CIRRHOSISR01DK039588 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI GERSHWIN, MERRILL E · 1988 to 2015
$2.0M
NIDDK NIH HHS DK067003NIDDK NIH HHS DK090019NIDDK NIH HHS DK39588NIDDK NIH HHS R01 DK039588NIDDK NIH HHS R01 DK067003NIDDK NIH HHS R01 DK090019NIDDK NIH HHS R37 DK039588
6 · The paper itself

Abstract

Data from genome wide association studies and geoepidemiological studies established that a combination of genetic predisposition and environmental stimulation is required for the loss of tolerance in primary biliary cholangitis (PBC). The serologic hallmark of PBC are the presence of high titer anti-mitochondrial autoantibodies (AMA) that recognize the lipoyl domain of the mitochondrial pyruvate dehydrogenase E2 (PDC-E2) subunit. Extensive efforts have been directed to investigate the molecular basis of AMA. Recently, experimental data has pointed to the thesis that the breaking of tolerance to PDC-E2 is a pivotal event in the initial etiology of PBC, including environmental xenobiotics including those commonly found in cosmetics and food additives, suggesting that chemical modification of the PDC-E2 epitope may render its vulnerable to become a neo-antigen and trigger an immune response in genetically susceptible hosts. Here, we will discuss the natural history, genetics and immunobiology of PBC and structural constraints of PDC-E2 in AMA recognition which makes it vulnerable to chemical modification.

Indexed as

AcetaminophenAnimalsAutoantibodiesAutoantigensChemical and Drug Induced Liver InjuryCholangitisDihydrolipoyllysine-Residue AcetyltransferaseDisease Models, AnimalHumansImmune ToleranceMiceMitochondriaMitochondrial ProteinsMolecular MimicryThioctic AcidXenobioticsAcetaminophenAutoantibodiesAutoantigensDihydrolipoyllysine-Residue AcetyltransferaseDLAT protein, humanMitochondrial ProteinsThioctic AcidXenobioticsAntimitochondrial autoantibodiesBreaking of tolerancePrimary biliary cholangitisPyruvate dehydrogenase E2Xenobiotics

Identifiers

PMID26755880
PMCPMC4698496
OpenAlexW2399073048

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.