HLA-DPB1 E69 genotype and exposure in beryllium sensitisation and disease

2021 ◽  
pp. oemed-2021-107736
Author(s):  
James Crooks ◽  
Margaret M Mroz ◽  
Michael VanDyke ◽  
Alison McGrath ◽  
Christine Schuler ◽  
...  
Keyword(s):  
Human Leukocyte ◽  
Environment Interaction ◽  
Lower Odds ◽  
Logistic Regression Models ◽  
Leukocyte Antigen ◽  
Exposure Response ◽  
Case Status ◽  
Over Dispersion ◽  
Beryllium Disease ◽  
Nested Case Control

ObjectivesHuman leukocyte antigen-DP beta 1 (HLA-DPB1) with a glutamic acid at the 69th position of the ß chain (E69) genotype and inhalational beryllium exposure individually contribute to risk of chronic beryllium disease (CBD) and beryllium sensitisation (BeS) in exposed individuals. This retrospective nested case–control study assessed the contribution of genetics and exposure in the development of BeS and CBD.MethodsWorkers with BeS (n=444), CBD (n=449) and beryllium-exposed controls (n=890) were enrolled from studies conducted at nuclear weapons and primary beryllium manufacturing facilities. Lifetime-average beryllium exposure estimates were based on workers’ job questionnaires and historical and industrial hygienist exposure estimates, blinded to genotype and case status. Genotyping was performed using sequence-specific primer-PCR. Logistic regression models were developed allowing for over-dispersion, adjusting for workforce, race, sex and ethnicity.ResultsHaving no E69 alleles was associated with lower odds of both CBD and BeS; every additional E69 allele increased odds for CBD and BeS. Increasing exposure was associated with lower odds of BeS. CBD was not associated with exposure as compared to controls, yet the per cent of individuals with CBD versus BeS increased with increasing exposure. No evidence of a gene-by-exposure interaction was found for CBD or BeS.ConclusionsRisk of CBD increases with E69 allele frequency and increasing exposure, although no gene by environment interaction was found. A decreased risk of BeS with increasing exposure and lack of exposure response in CBD cases may be due to the limitations of reconstructed exposure estimates. Although reducing exposure may not prevent BeS, it may reduce CBD and the associated health effects, especially in those carrying E69 alleles.

scholarly journals The increased risk of multiple sclerosis associated with HLA-DRB1*15:01 and smoking is modified by alcohol consumption

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anna Karin Hedström ◽  
Tomas Olsson ◽  
Lars Alfredsson
Keyword(s):  
Multiple Sclerosis ◽  
Alcohol Consumption ◽  
Human Leukocyte ◽  
Population Based ◽  
Inverse Association ◽  
Swedish Population ◽  
Logistic Regression Models ◽  
Leukocyte Antigen ◽  
Increased Risk ◽  
Incident Cases

AbstractPrevious studies have observed an inverse association between alcohol consumption and multiple sclerosis (MS) risk. We aimed to investigate possible interactions between alcohol consumption, MS-associated human leukocyte antigen (HLA) genes and smoking regarding MS risk. We used a Swedish population-based case–control study (2059 incident cases, 2887 controls) matched by age, sex, and residential area. Subjects with different genotypes and alcohol consumption habits were compared regarding MS risk, by calculating odds ratios with 95% confidence intervals using logistic regression models. Interaction on the additive scale between non-drinking and both genotype and smoking were assessed by calculating the attributable proportion due to interaction (AP). There was a dose-dependent inverse association between alcohol consumption and MS risk (p for trend < 0.0001). A potentiating effect was observed between non-drinking and presence of DRB1*15:01 (AP 0.3, 95% CI 0.2–0.5) which was of similar magnitude irrespective of smoking habits. Non-drinking also interacted with smoking to increase MS risk (AP 0.2, 95% CI 0.06–0.4). Non-drinking interacts with DRB1*15:01 and smoking to increase the risk of MS. Better understanding of the mechanisms behind our findings may help to define ways to achieve protection against MS by other means than alcohol consumption.

scholarly journals Human leukocyte antigen class II variants and adult-onset asthma: does occupational allergen exposure play a role?

2014 ◽  
Vol 44 (5) ◽  
pp. 1234-1242 ◽  
Author(s):  
Lidwien A.M. Smit ◽  
David P. Strachan ◽  
Roel Vermeulen ◽  
Paul I.W. de Bakker ◽  
Florence Demenais ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Association Studies ◽  
Human Leukocyte ◽  
Occupational Exposures ◽  
Class Ii ◽  
Environment Interaction ◽  
Genome Wide Association Studies ◽  
Adult Onset ◽  
Leukocyte Antigen ◽  
Hla Dq

Recently, a locus centred on rs9273349 in the HLA-DQ region emerged from genome-wide association studies of adult-onset asthma. We aimed to further investigate the role of human leukocyte antigen (HLA) class II in adult-onset asthma and a possible interaction with occupational exposures.We imputed classical HLA-II alleles from 7579 single-nucleotide polymorphisms in 6025 subjects (1202 with adult-onset asthma) from European cohorts: ECRHS, SAPALDIA, EGEA and B58C, and from surveys of bakers and agricultural workers. Based on an asthma-specific job–exposure matrix, 2629 subjects had ever been exposed to high molecular weight (HMW) allergens. We explored associations between 23 common HLA-II alleles and adult-onset asthma, and tested for gene–environment interaction with occupational exposure to HMW allergens. Interaction was also tested for rs9273349.Marginal associations of classical HLA-II alleles and adult-onset asthma were not statistically significant. Interaction was detected between the DPB1*03:01 allele and exposure to HMW allergens (p = 0.009), in particular to latex (p = 0.01). In the unexposed group, the DPB1*03:01 allele was associated with adult-onset asthma (OR 0.67, 95%CI 0.53–0.86). HMW allergen exposures did not modify the association of rs9273349 with adult-onset asthma.Common classical HLA-II alleles were not marginally associated with adult-onset asthma. The association of latex exposure and adult-onset asthma may be modified by DPB1*03:01.

Human leukocyte antigen-DR15, low infant sibling exposure and multiple sclerosis: Gene-environment interaction

2010 ◽  
Vol 67 (2) ◽  
pp. 261-265 ◽  
Author(s):  
Ingrid A. F. van der Mei ◽  
Arine-Louise Ponsonby ◽  
Bruce V. Taylor ◽  
Jim Stankovich ◽  
Joanne L. Dickinson ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Environment Interaction ◽  
Leukocyte Antigen ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Infant Sibling

Role of Human Leukocyte Antigen-DP in the Presentation of Beryllium to T Cells in Chronic Beryllium Disease

CHEST Journal ◽  
2001 ◽  
Vol 120 (1) ◽  
pp. S58
Author(s):  
Andrew P. Fontenot ◽  
Michaelann Vollmer ◽  
Lee S. Newman ◽  
Brian L. Kotzin
Keyword(s):  
T Cells ◽  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Chronic Beryllium Disease ◽  
Leukocyte Antigen ◽  
Beryllium Disease

scholarly journals Genetic Associations between Delusional Disorder and Paranoid Schizophrenia: A Novel Etiologic Approach

2006 ◽  
Vol 51 (6) ◽  
pp. 342-349 ◽  
Author(s):  
Monojit Debnath ◽  
Sujit K Das ◽  
Nirmal K Bera ◽  
Chitta R Nayak ◽  
Tapas K Chaudhuri
Keyword(s):  
Paranoid Schizophrenia ◽  
Human Leukocyte ◽  
Hla Class I ◽  
Delusional Disorder ◽  
Genetic Associations ◽  
Typing Method ◽  
Leukocyte Antigen ◽  
Hla Genes ◽  
Molecular Typing Method ◽  
Nested Case Control

Objectives: Genetic associations between delusional disorder and paranoid schizophrenia are not well understood, although involvement of biological factors has been suspected. We investigated the incidence of human leukocyte antigen (HLA) class I alleles in patients with delusional disorder and paranoid schizophrenia, first, to explore a possible immunogenetic etiology of these paranoid disorders and, second, to determine whether they share similar etiologic mechanisms. Method: We employed a nested case–control study design. Psychiatric reference data were available for 38500 patients attending a hospital-based psychiatric outpatient department between 1998 and 2005. We enrolled 100 patients with delusional disorder and 50 patients with paranoid schizophrenia as the subject cases, using DSM-IV criteria. We considered equivalent numbers of healthy volunteers matched for age and ethnic background as control subjects. All subjects came from an India-born Bengali population. We applied the polymerase chain reaction–based molecular typing method to all patients and healthy subjects. Results: The HLA-A*03 gene is significantly associated with delusional disorder as well as with paranoid schizophrenia. This HLA gene alone or in linkage disequilibrium with other HLA genes or other closely linked non-HLA genes may influence susceptibility to delusional disorder and paranoid schizophrenia. Conclusions: The study reveals important associations between HLA genes and paranoid disorders. Delusional disorder and paranoid schizophrenia may share similar etiologic mechanisms. This preliminary observation may help our understanding of the genetic basis of these paranoid disorders.

Abstract # OR-8: Serum 25-Hydroxyvitamin D Associates with Human Leukocyte Antigen (HLA) Polymorphisms

2016 ◽  
Vol 22 ◽  
pp. 6
Author(s):  
Leena Kinnunen ◽  
Valma Harjutsalo ◽  
Heljä-Marja Surcel ◽  
Christel Lamberg-Allardt ◽  
Jaakko Tuomilehto ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D

Human Leukocyte Antigen Mismatch and Other Factors Affecting Cryopreserved Allograft Valve Function

2008 ◽  
Vol 11 (1) ◽  
pp. E42-E45 ◽  
Author(s):  
Cheng-Hon Yap ◽  
Peter D. Skillington ◽  
George Matalanis ◽  
Bruce B. Davis ◽  
Brian D. Tait ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Factors Affecting ◽  
Leukocyte Antigen ◽  
Valve Function
Sign in / Sign up

Export Citation Format

Share Document