Evidence map›Paper›PMID 20975735›Full record

ReviewImmunology and cell biology2011

The autoimmunity of primary biliary cirrhosis and the clonal selection theory.

Carlo Selmi, Ian R Mackay, M Eric Gershwin

Abstract readReview
In one paragraph

Review in Immunology and cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Molecular mechanisms of hepatic apoptosis.Cell death & disease · 2014
    Review
  8. Article
  9. Diagnosis of Liver Involvement in Primary Sjögren Syndrome.Journal of clinical and translational hepatology · 2013
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. 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

3 authors.

Carlo SelmiDivision of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA 95616, USA.
Ian R Mackay
M Eric Gershwin

Funding

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 DK39588NIDDK NIH HHS R01 DK039588NIDDK NIH HHS R37 DK039588
6 · The paper itself

Abstract

Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease in which an immune-mediated injury targets the small intrahepatic bile ducts. PBC is further characterized by highly specific serum antimitochondrial autoantibodies (AMAs) and autoreactive T cells, a striking female predominance, a strong genetic susceptibility and a plethora of candidate environmental factors to trigger the disease onset. For these reasons, PBC appears ideal to represent the developments of the clonal selection theory over the past decades. First, a sufficiently potent autoimmunogenic stimulus in PBC would require the coexistence of numerous pre-existing conditions (mostly genetic, as recently illustrated by genome-wide association studies and animal models) to perpetuate the destruction of the biliary epithelium by the immune system via the persistence of forbidden clones. Second, the proposed modifications of mitochondrial autoantigens caused by infectious agents and/or xenobiotics well illustrate the possibility that peculiar changes in the antigen structure and flexibility may contribute to tolerance breakdown. Third, the unique apoptotic features shown for cholangiocytes are the ideal setting for the development of mitochondrial autoantigen presentation to the immune system through macrophages and AMA; thus, turning the non-traditional mitochondrial antigen into a traditional one. This article will review the current knowledge on PBC etiology and pathogenesis in light of the clonal selection theory developments.

Indexed as

AnimalsAutoantibodiesAutoantigensAutoimmunityClonal DeletionDihydrolipoyllysine-Residue AcetyltransferaseEpitopesHumansImmunity, InnateLiver Cirrhosis, BiliaryMitochondriaThioctic AcidAutoantibodiesAutoantigensDihydrolipoyllysine-Residue AcetyltransferaseEpitopesThioctic Acid

Identifiers

PMID20975735
PMCPMC3017230

What OpenQuestion holds

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Registered trials

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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.