ArticleWorld journal of hepatology2011
Genetic susceptibility to autoimmune liver disease.
Article in World journal of hepatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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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.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Identifying the genetic link between type 1 diabetes and autoimmune liver diseases.Clinical and experimental hepatology · 2025Article
- PD-L1 expression levels in mesenchymal stromal cells predict their therapeutic values for autoimmune hepatitis.Stem cell research & therapy · 2023Article
- Stem cell therapies for autoimmune hepatitis.Stem cell research & therapy · 2021Review
- Animal Models of Autoimmune Liver Diseases: a Comprehensive Review.Clinical reviews in allergy & immunology · 2020Review
- Natural evolution of hepatitis C virus infection in hemodialysis Tunisian patients and CTLA-4 SNP's.World journal of gastroenterology · 2015Article
- Inhibition of autoimmune Chagas-like heart disease by bone marrow transplantation.PLoS neglected tropical diseases · 2014Article
- Epidemiological Dynamics of Burden and Health Inequalities in Metabolic Dysfunction-associated Steatotic Liver Disease in Adolescents at Global, Regional, and National Levels, 1990-2021.Journal of clinical and experimental hepatologyArticle
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC) are considered as putative autoimmune diseases of the liver. Whereas strong evidence that bacterial infection may trigger PBC exists, the etiologies for PSC and AIH remain unknown. Although there have been significant discoveries of genetic polymorphisms that may underlie the susceptibility to these liver diseases, their associations with environmental triggers and the subsequent implications have been difficult to elucidate. While single nucleotide polymorphisms within the negative costimulatory molecule cytotoxic T lymphocyte antigen 4 (CTLA-4) have been suggested as genetic susceptibility factors for all three disorders, we discuss the implications of CTLA-4 susceptibility alleles mainly in the context of PBC, where Novosphingobium aromaticivorans, an ubiquitous alphaproteobacterium, has recently been specifically associated with the pathogenesis of this devastating liver disease. Ultimately, the discovery of infectious triggers of PBC may expand the concept of genetic susceptibility in immune-mediated liver diseases from the concept of aberrant immune responses against self-antigens to insufficient and/or inappropriate immunological defense mechanisms allowing microbes to cross natural barriers, establish infection and damage respective target organs.
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Registered trials
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.