ArticleMolecular biology reports2014
HLA DQB1 alleles are related with nonalcoholic fatty liver disease.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Association Between HLA Polymorphisms and Non-Alcoholic Fatty Liver Disease in Patients with Rheumatoid Arthritis: An Observational Study.Diseases (Basel, Switzerland) · 2026Article
- Dietary contributions in the genetic variation of liver fibrosis: a genome-wide association study of fibrosis-4 index in the liver fibrosis development.Cell & bioscience · 2024Article
- Integrative network-based analysis on multiple Gene Expression Omnibus datasets identifies novel immune molecular markers implicated in non-alcoholic steatohepatitis.Frontiers in endocrinology · 2023Article
- Machine learning identifies ferroptosis-related gene ANXA2 as potential diagnostic biomarkers for NAFLD.Frontiers in endocrinology · 2023Article
- The transcriptome-wide association search for genes and genetic variants which associate with BMI and gestational weight gain in women with type 1 diabetes.Molecular medicine (Cambridge, Mass.) · 2021Article
- Genome-Wide Association Study of Lean Nonalcoholic Fatty Liver Disease Suggests Human Leukocyte Antigen as a Novel Candidate Locus.Hepatology communications · 2020Article
- Analysis of human leukocyte antigen allele polymorphism in patients with non alcoholic fatty liver disease.Medicine · 2019Observational
- Transcriptional Network Analysis Implicates Altered Hepatic Immune Function in NASH development and resolution.Nature metabolism · 2019Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease. NAFLD is a complex disease and inflammation is a crucial component in the disease pathogenesis. Recent genome wide association studies in hepatology area highlighted significant relations with human leukocyte antigen (HLA) DQ region and certain liver diseases. The previous animal models also emphasized the involvement of adaptive immune system in the liver damage pathways. To investigate possible polymorphisms in the HLA region that can contribute to the immune response affecting the NAFLD, we enrolled 93 consecutive biopsy proven NAFLD patients and a control group consisted of 101 healthy people and genotyped HLA DQB1 alleles at high resolution by sequence specific primers-polymerase chain reaction. The mean NAFLD activity score (NAS) was 5.2 ± 1.2, fibrosis score was 0.9 ± 0.9, ALT was 77 ± 47.4 U/L, AST was 49.4 ± 26.3 U/L. Among 13 HLA DQB1 alleles analyzed in this study, DQB1*06:04 was observed significantly at a more frequent rate among the NAFLD patients compared to that of healthy controls (12.9 vs. 2 % χ(2) = 8.6, P = 0.003, P c = 0.039, OR: 7.3 95 % CI 1.6-33.7). In addition, the frequency of DQB1*03:02 was significantly higher in the healthy control group than the NAFLD patients (24.8 vs. 7.5 %, χ(2) = 10.4, P = 0.001, P c = 0.013, OR: 0.2, 95 % CI 0.1-0.6). NAFLD patients were grouped according to their fibrosis score and NAS. The distribution of DQB1 alleles over stratified NAFLD patients did not reveal any statistically significant relation. Taken together, immune repertoire of individuals may have an effect on NAFLD pathogenesis and therefore, in NAFLD, adaptive immunity pathways should be investigated.
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