A new risk factor for the development of non-alcoholic fatty liver disease: HLA complex genes

Celıkbılek, Mehmet; Şelçuk, Haldun; Yilmaz, Uğur

doi:10.4318/tjg.2011.0237

Cited by 13 publications

(11 citation statements)

References 30 publications

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“…This result strongly suggests that the modification in MHC II gene expression affected neither ALT nor AST levels, consistent to their comparable liver histology between groups. It has been, however, suggested that some alleles in MHC II pathway were associated with a severity of NAFLD and ALT, but not AST levels, in a Turkish population [33]. In this study, the investigators could not assess a presence of NASH in the population.…”

Section: Discussionmentioning

confidence: 83%

Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice

Willemin

Roger

Bauduret

et al. 2013

International Journal of Endocrinology

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Single-nucleotide polymorphisms within major histocompatibility class II (MHC II) genes have been associated with an increased risk of drug-induced liver injury. However, it has never been addressed whether the MHC II pathway plays an important role in the development of nonalcoholic fatty liver disease, the most common form of liver disease. We used a mouse model that has a complete knockdown of genes in the MHC II pathway (MHCIIΔ/Δ). Firstly we studied the effect of high-fat diet-induced hepatic inflammation in these mice. Secondly we studied the development of carbon-tetra-chloride- (CCl4-) induced hepatic cirrhosis. After the high-fat diet, both groups developed obesity and hepatic steatosis with a similar degree of hepatic inflammation, suggesting no impact of the knockdown of MHC II on high-fat diet-induced inflammation in mice. In the second study, we confirmed that the CCl4 injection significantly upregulated the MHC II genes in wild-type mice. The CCl4 treatment significantly induced genes related to the fibrosis formation in wild-type mice, whereas this was lower in MHCIIΔ/Δ mice. The liver histology, however, showed no detectable difference between groups, suggesting that the MHC II pathway is not required for the development of hepatic fibrosis induced by CCl4.

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Section: Discussionmentioning

confidence: 83%

Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice

Willemin

Roger

Bauduret

et al. 2013

International Journal of Endocrinology

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“…[15–17] HLA loci are highly polymorphic and may confer greater risk for NASH and NASH-related cirrhosis. [2,4,5] In the present study, we have examined for genetic predisposition for NASH and advanced fibrosis within the HLA loci among biopsy-proven NAFLD and its subtypes.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, HLA-B∗65 has been shown to be independently associated with the development of NAFLD. [2] Furthermore, HLA-B∗35 and -B∗40 have been linked to the development of cirrhosis in patients with alcoholic fatty liver disease. [3–5] Within the HLA class II, HLA- DQ5 has been significantly associated with NAFLD.…”

Section: Introductionmentioning

confidence: 99%

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Analysis of human leukocyte antigen allele polymorphism in patients with non alcoholic fatty liver disease

et al. 2019

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The human leukocyte antigen (HLA) genes may play a role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and its progressive form, non-alcoholic steatohepatitis (NASH). The aim of this study was to assess the association of HLA class I and II alleles with NASH and its histological features. Deoxyribonucleic acid (DNA) was extracted from 140 subjects (85 biopsy-proven NAFLD and 55 controls) and genotyped for HLA (-A, -B, -C, -DR1, -DR3, -DQ, and -DP). Liver biopsies were assessed for presence of NASH, degree of fibrosis and inflammation. Multivariate analysis was performed to assess associations between HLA genes and different histologic features of NAFLD. Our data for HLA class I showed that HLA-C∗4 was associated with lower risk for histologic NASH and HLA-C∗6 was protective against portal fibrosis. Conversely, HLA-B∗27 was associated with high-grade hepatic steatosis, while HLA-A∗31 was associated with increased risk for advanced fibrosis. Among HLA class II alleles, HLA-DQA1∗01 was associated with lower risk for NASH while HLA-DRB1∗03 was associated with increased risk for NASH. Our findings indicate that HLA class I and II gene polymorphism may be associated with susceptibility to NASH, fibrosis and other pathologic features and may be involved in the pathogenesis of NAFLD.

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“…On the other hand, HLA-DRB1*04, HLA-DQB1*0401/2, and TNFA*1 (-308) were associated with disease resistance [2]. Furthermore, initial studies on the role of genetic factors in susceptibility to non-alcoholic fatty liver disease point toward an important role of human leukocyte antigen in the pathogenesis of non-alcoholic fatty liver disease [3].…”

Section: To the Editormentioning

confidence: 99%

Host factors and typhoid fever-associated intestinal perforation in children in Nigeria

Arya

Agarwal

2012

Pediatr Surg Int

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A new risk factor for the development of non-alcoholic fatty liver disease: HLA complex genes

Cited by 13 publications

References 30 publications

Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice

Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice

Analysis of human leukocyte antigen allele polymorphism in patients with non alcoholic fatty liver disease

Host factors and typhoid fever-associated intestinal perforation in children in Nigeria

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