Evidence map›Paper›PMID 25701076›Full record

ArticleJournal of autoimmunity2015

Systems biologic analysis of T regulatory cells genetic pathways in murine primary biliary cirrhosis.

Yin-Hu Wang, Wei Yang, Jing-Bo Yang, Yan-Jie Jia, Wei Tang, M Eric Gershwin, William M Ridgway, Zhe-Xiong Lian

Abstract read
In one paragraph

Article in Journal of autoimmunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. The aryl hydrocarbon receptor in liver inflammation.Seminars in immunopathology · 2021
    Review
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  8. Animal Models of Autoimmune Liver Diseases: a Comprehensive Review.Clinical reviews in allergy & immunology · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Trichloroethylene Exposure Reduces Liver Injury in a Mouse Model of Primary Biliary Cholangitis.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    Article
  18. Article
  19. Article
  20. 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 3 institutions in 2 countries.

Yin-Hu WangLiver Immunology Laboratory, Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: wangyh8@mail.ustc.edu.cn.
Wei YangLiver Immunology Laboratory, Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: ywei0702@mail.ustc.edu.cn.
Jing-Bo YangLiver Immunology Laboratory, Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: yjingb@mail.ustc.edu.cn.
Yan-Jie JiaLiver Immunology Laboratory, Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: jyanjie@mail.ustc.edu.cn.
Wei TangLiver Immunology Laboratory, Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China. Electronic address: wayne012@mail.ustc.edu.cn.
M Eric GershwinDivision of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA 95616, USA. Electronic address: megershwin@ucdavis.edu.
William M RidgwayDivision of Immunology, Allergy and Rheumatology, University of Cincinnati, Cincinnati, OH 45220, USA. Electronic address: wridg1@gmail.com.
Zhe-Xiong LianLiver Immunology Laboratory, Institute of Immunology and The CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China; Innovation Center for Cell Biology, Hefei National Laboratory for Physical Sciences at Microscale, Hefei, Anhui 230027, China. Electronic address: zxlian1@ustc.edu.cn.
University of Science and Technology of China · CNUniversity of California, Davis · USUniversity of Cincinnati · US

Funding

dnTGF Beta RII Mice and PBCR01DK090019 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GERSHWIN, MERRILL E, RIDGWAY, WILLIAM M · 2010 to 2017
$3.8M
NIDDK NIH HHS DK090019NIDDK NIH HHS R01 DK090019
6 · The paper itself

Abstract

CD4(+)Foxp3(+) regulatory T cells (Tregs) play a non-redundant role in control of excessive immune responses, and defects in Tregs have been shown both in patients and murine models of primary biliary cirrhosis (PBC), a progressive autoimmune biliary disease. Herein, we took advantage of a murine model of PBC, the dominant negative transforming growth factor β receptor II (dnTGFβRII) mice, to assess Treg genetic defects and their functional effects in PBC. By using high-resolution microarrays with verification by PCR and protein expression, we found profound and wide-ranging differences between dnTGFβRII and normal, wild type Tregs. Critical transcription factors were down-regulated including Eos, Ahr, Klf2, Foxp1 in dnTGFβRII Tregs. Functionally, dnTGFβRII Tregs expressed an activated, pro-inflammatory phenotype with upregulation of Ccl5, Granzyme B and IFN-γ. Genetic pathway analysis suggested that the primary effect of loss of TGFβ pathway signaling was to down regulate immune regulatory processes, with a secondary upregulation of inflammatory processes. These findings provide new insights into T regulatory genetic defects; aberrations of the identified genes or genetic pathways should be investigated in human PBC Tregs. This approach which takes advantage of biologic pathway analysis illustrates the ability to identify genes/pathways that are affected both independently and dependent on abnormalities in TGFβ signaling. Such approaches will become increasingly useful in human autoimmunity.

Indexed as

AnimalsChemokine CCL5Disease Models, AnimalFemaleForkhead Transcription FactorsGene Expression RegulationGranzymesHumansInflammation MediatorsInterferon-gammaLiver Cirrhosis, BiliaryMiceMice, Mutant StrainsMicroarray AnalysisMutationProtein Serine-Threonine KinasesChemokine CCL5Forkhead Transcription FactorsFoxp3 protein, mouseGranzymesInflammation MediatorsInterferon-gammaProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITranscription FactorsCholangitisPrimary biliary cirrhosisRegulatory T cellsTranscription profile and pathway analysis

Identifiers

PMID25701076
PMCPMC4829434
OpenAlexW2081901155

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.