HLA DQB1 alleles are related with nonalcoholic fatty liver disease

Levent Doganay*, Seyma Katrinli, Yasar Colak, Ebubekir Senates, Ebru Zemheri, Oguzhan Ozturk, Feruze Yilmaz Enc, Ilyas Tuncer, Gizem Dinler Doganay

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


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 % χ2 = 8.6, P = 0.003, Pc = 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 %, χ2 = 10.4, P = 0.001, Pc = 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.

Original languageEnglish
Pages (from-to)7937-7943
Number of pages7
JournalMolecular Biology Reports
Issue number12
Publication statusPublished - 1 Dec 2014

Bibliographical note

Publisher Copyright:
© 2014, Springer Science+Business Media Dordrecht.


This study is supported by internal research funds of Istanbul Technical University.

FundersFunder number
Istanbul Teknik Üniversitesi


    • HLA DQ
    • Inflammation
    • Liver
    • Nonalcoholic fatty liver disease (NAFLD)
    • Nonalcoholic steatohepatitis (NASH)


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