Evidence map›Paper›PMID 23991203›Full record

ArticlePloS one2013

B cell deficient mice are protected from biliary obstruction in the rotavirus-induced mouse model of biliary atresia.

Amy G Feldman, Rebecca M Tucker, Erika K Fenner, Roberta Pelanda, Cara L Mack

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
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  3. Biliary atresia.Nature reviews. Disease primers · 2024
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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 3 institutions in 1 country.

Amy G FeldmanDepartment of Pediatrics, Section of Pediatric Gastroenterology, Children's Hospital, Colorado, Aurora, Colorado, USA. afeldman@luriechildrens.org
Rebecca M Tucker
Erika K Fenner
Roberta Pelanda
Cara L Mack
University of Colorado Denver · USChildren's Hospital Colorado · USNational Jewish Health · US

Funding

Tolerance in Polyclonal and Oligoclonal Immune SystemsR01AI052310 · NIAID · UNIVERSITY OF COLORADO DENVER · PI PELANDA, ROBERTA · 2003 to 2017
$5.0M
T Cell-Mediated Mechanisms of Autoimmunity in Murine and Human Biliary AtresiaR01DK078195 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI MACK, CARA LYNN · 2007 to 2011
$1.5M
NIAID NIH HHS R01 AI052310NIDDK NIH HHS 1 RO1 DK078195NIDDK NIH HHS R01 DK078195NIDDK NIH HHS T32-DK06700907
6 · The paper itself

Abstract

A leading theory regarding the pathogenesis of biliary atresia (BA) is that bile duct injury is initiated by a virus infection, followed by an autoimmune response targeting bile ducts. In experimental models of autoimmune diseases, B cells have been shown to play an important role. The aim of this study was to determine the role of B cells in the development of biliary obstruction in the Rhesus rotavirus (RRV)-induced mouse model of BA. Wild-type (WT) and B cell-deficient (Ig-α(-/-)) mice received RRV shortly after birth. Ig-α(-/-) RRV-infected mice had significantly increased disease-free survival rate compared to WT RRV-infected BA mice (76.8% vs. 17.5%). In stark contrast to the RRV-infected BA mice, the RRV-infected Ig-α(-/-) mice did not have hyperbilirubinemia or bile duct obstruction. The RRV-infected Ig-α(-/-) mice had significantly less liver inflammation and Th1 cytokine production compared to RRV-infected WT mice. In addition, Ig-α(-/-) mice had significantly increased numbers of regulatory T cells (Tregs) at baseline and after RRV infection compared to WT mice. However, depletion of Tregs in Ig-α(-/-) mice did not induce biliary obstruction, indicating that the expanded Tregs in the Ig-α(-/-) mice were not the sole reason for protection from disease. Conclusion : B cell deficient Ig-α(-/-) mice are protected from biliary obstruction in the RRV-induced mouse model of BA, indicating a primary role of B cells in mediating disease pathology. The mechanism of protection may involve lack of B cell antigen presentation, which impairs T-cell activation and Th1 inflammation. Immune modulators that inhibit B cell function may be a new strategy for treatment of BA.

Indexed as

AnimalsAntigen-Presenting CellsBiliary AtresiaB-LymphocytesCholestasisDisease Models, AnimalFlow CytometryMiceRotavirusT-Lymphocytes, Regulatory

Identifiers

PMID23991203
PMCPMC3749125
OpenAlexW2043362229

What OpenQuestion holds

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LicenceCC BY
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.