Objective: Susceptibility to autoimmune hepatitis (AIH) type 1 has been associated with DRB1*03, DRB1*04, and DRB3 alleles in European and North-American whites, with DRB1*04 in Japan, and with DRB1*04 and DRB1*13 in Latin America. Very few studies have been performed on AIH type 2. The aim of the present study was to evaluate the association of AIH types 1 and 2 with HLA-DR and DQ loci.
Methods: We performed HLA-DRB and -DQB1 typing by polymerase chain reaction amplification with sequence-specific primers (PCR-SSP) in 139 AIH patients. Most had AIH type 1 associated with circulating anti-smooth muscle antibody with F-actin specificity or antinuclear antibody. Twenty-eight patients presented AIH type 2 with anti-liver/kidney microsome type 1 or anti-liver cytosol type 1 antibodies.
Results: We observed a significant increase of DRB1*13 (70% vs 26% of controls, p < 0.00001) and DRB3 (93% vs 69% of controls, p < 0.00001) in AIH type 1 patients. Analysis of patients without DRB1*13 disclosed a secondary association with DRB1*03 (70% vs 30% of controls, p = 0.0001) and either the DRB1*13 or the DRB1*03 alleles were present in the majority of these patients (91% vs 48% of controls, p = 0.001). Comparison of DRB1*13- and DRB1*03-positive subjects revealed that the former alleles conferred susceptibility to younger patients with AIH type 1. DQB1 typing showed a significant increase in DQB1*06 (68% vs 41% of controls, p = 0.00007) in strong linkage disequilibrium with DRB1*13, and a decrease in DQB1*0301 (8% vs 47% of controls, p(c) = 0.0003). On the other hand, HLA typing of patients with AIH type 2 disclosed a significant increase in the DRB1*07 (68% vs 20% of controls, p(c) < 0.00014), DRB4 (79% vs 43% of controls, p(c) = 0.004), and DQB1*02 (86% vs 42%, p = 0.00002) alleles. After exclusion of DRB1*07, a secondary association with HLA-DRB1*03 was further observed in these patients (78% vs 30%, p = 0.007) and most of them had either DRB1*07 or DRB1*03 (93% vs 44% of controls, p(c) < 0.0001).
Conclusions: Our data indicate that predisposition to AIH types 1 and 2 is associated, respectively, with the DRB1*13 or DRB1*03 and DRB1*07 or DRB1*03 alleles, and suggest that protection against type 1 disease may be conferred by DQB1*0301. In addition, the cluster of DRB1*13 in children with AIH type 1 also supports the concept that different HLA alleles might influence the onset of the disease.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1572-0241.1999.01229.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Regulation of Concanavalin A-induced Immune Hepatitis in Mice by Dihydromyricetin at the M1/M2 Type Macrophage Level.
Discov Med
January 2025
Department of General Surgery, Section for Day Surgery, The Third People's Hospital of Chengdu, Affiliated Hospital of Southwest Jiaotong University & The Second Affiliated Hospital of Chengdu, Chongqing Medical University, 610031 Chengdu, Sichuan, China.
Background: Autoimmune hepatitis (AIH) is an autoimmune disease accompanied by an autoimmune inflammatory response that often leads to severe liver damage. In addition, it may further lead to complications such as liver fibrosis, cirrhosis and liver failure. Dihydromyricetin (DHM) possesses various pharmacological properties, such as being anti-inflammatory, antioxidant, and antibacterial.
View Article and Find Full Text PDFGlucocorticoid receptors: The key of the response to steroid therapy in autoimmune hepatitis.
Clin Exp Hepatol
March 2024
Department of Pediatric Hepatology, Gastroenterology and Nutrition, National Liver Institute, Menoufia University, Shebin El-Kom, Menoufia, Egypt.
Aim Of The Study: This study was performed to investigate the hepatic expression of glucocorticoid receptors (GR) and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in pediatric autoimmune hepatitis (AIH) patients and its relation to the steroid response.
Material And Methods: This study included 100 patients diagnosed with AIH on immunosuppressive therapy with different responses to treatment. The patients were subjected to full history taking and thorough clinical examination, laboratory investigations, abdominal ultrasound and liver biopsy for histopathological evaluation and assessment of the hepatic expression of GR and 11β-HSD1.
A genome-wide cross-trait analysis identifying shared genetic basis and causal relationships between Hunner-type interstitial cystitis and autoimmune diseases in East Asian populations.
Front Immunol
December 2024
Department of Urology, Lab of Health Data Science, Innovation Institute for Integration of Medicine and Engineering, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Article Synopsis
- The study explores the genetic connections between Hunner interstitial cystitis (HIC) and autoimmune diseases (ADs), suggesting they may share common genetic factors.
- Utilizing a large East Asian population, the researchers employed advanced statistical methods like Mendelian randomization to assess causal relationships and identify genetic markers linked to both conditions.
- Results showed causal effects of certain autoimmune conditions on HIC and vice versa, along with insights into genetic variants affecting gene expression in autoimmune-related tissues, highlighting a potential shared genetic basis for these diseases.
IFITM1 aggravates ConA-Induced autoimmune hepatitis by promoting NKT cell activation through increased AMPK-Dependent mitochondrial function.
Int Immunopharmacol
January 2025
Medical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 10020, China; Department of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China. Electronic address:
Although interferon-induced transmembrane 1 (IFITM1) is known for its crucial role in antiviral immunity, its involvement in autoimmune hepatitis (AIH) remains largely unexplored. In this study, we observed that IFITM1 expression is markedly upregulated in a Concanavalin A (ConA)-induced AIH model, with particularly high and markedly elevated expression in natural killer T (NKT) cells. To further understand the role of IFITM1, we examined the responses of IFITM1 mice in a model of ConA-induced liver injury.
View Article and Find Full Text PDFAcute intermittent hypoxia elicits sympathetic neuroplasticity independent of peripheral chemoreflex activation and spinal cord tissue hypoxia in a rodent model of high-thoracic spinal cord injury.
Exp Neurol
February 2025
International Collaboration on Repair Discoveries, University of British Columbia, Vancouver, BC, Canada; Centre for Chronic Disease Prevention and Management, University of British Columbia, Kelowna, BC, Canada; Department of Cellular and Physiological Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. Electronic address:
Article Synopsis
- The study investigates how spinal cord injury (SCI) impacts the body's ability to control heart and blood vessels, leading to cardiovascular diseases (CVD) due to loss of medullary control.
- It explores acute intermittent hypoxia (AIH) as a potential treatment to stimulate sympathetic nerve activity and promote neuroplastic changes called long-term facilitation (LTF) in the sympathetic circuits after SCI.
- Results show that a single session of AIH can effectively boost sympathetic nerve activity in a rat model of SCI, opening possibilities for chronic AIH treatment to manage complications from sympathetic hypoactivity.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!