ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Chronic beryllium disease, HLA-DPB1, and the DP peptide binding groove.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- HLA-DPB1 E69 genotype and exposure in beryllium sensitisation and disease.Occupational and environmental medicine · 2022Article
- Pulmonary granulomatosis of genetic origin.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Multiplexed gene expression analysis of HLA class II-associated podoconiosis implicates chronic immune activation in its pathogenesis.Transactions of the Royal Society of Tropical Medicine and Hygiene · 2020Article
- Adaptive Immunity in Pulmonary Sarcoidosis and Chronic Beryllium Disease.Frontiers in immunology · 2020Review
- Protective role of B cells in sterile particulate-induced lung injury.JCI insight · 2019Article
- DNA Methylation Changes in Lung Immune Cells Are Associated with Granulomatous Lung Disease.American journal of respiratory cell and molecular biology · 2019Article
- HLA-DPNature communications · 2017Article
- Identification of Functional and Expression Polymorphisms Associated With Risk for Antineutrophil Cytoplasmic Autoantibody-Associated Vasculitis.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- The orthologs of HLA-DQ and -DP genes display abundant levels of variability in macaque species.Immunogenetics · 2017Article
- Article
- Genetic risk of extranodal natural killer T-cell lymphoma: a genome-wide association study.The Lancet. Oncology · 2016Article
- Research to Practice Implications of High-Risk Genotypes for Beryllium Sensitization and Disease.Journal of occupational and environmental medicine · 2016Article
- Beryllium-Induced Hypersensitivity: Genetic Susceptibility and Neoantigen Generation.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- Immunogenetics of Disease-Causing Inflammation in Sarcoidosis.Clinical reviews in allergy & immunology · 2015Review
- Gene-environment interaction from international cohorts: impact on development and evolution of occupational and environmental lung and airway disease.Seminars in respiratory and critical care medicine · 2015Review
- Chronic Beryllium Disease: revealing the role of beryllium ion and small peptides binding to HLA-DP2.PloS one · 2014Article
- Human leukocyte antigen class II haplotypes affect clinical characteristics and progression of type 1 autoimmune hepatitis in Japan.PloS one · 2014Article
- T cell recognition of beryllium.Current opinion in immunology · 2013Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
Multiple epidemiologic studies demonstrate associations between chronic beryllium disease (CBD), beryllium sensitization (BeS), and HLA-DPB1 alleles with a glutamic acid residue at position 69 (E69). Results suggest that the less-frequent E69 variants (non-*0201/*0202 alleles) might be associated with greater risk of CBD. In this study, we sought to define specific E69-carrying alleles and their amino acid sequences in the DP peptide binding groove, as well as their relationship to CBD and BeS risk, using the largest case control study to date. We enrolled 502 BeS/CBD subjects and 653 beryllium-exposed controls from three beryllium industries who gave informed consent for participation. Non-Hispanic white cases and controls were frequency-matched by industry. HLA-DPB1 genotypes were determined using sequence-specific primer PCR. The E69 alleles were tested for association with disease individually and grouped by amino acid structure using logistic regression. The results show that CBD cases were more likely than controls to carry a non-*02 E69 allele than an *02 E69, with odds ratios (95% confidence interval) ranging from 3.1 (2.1-4.5) to 3.9 (2.6-5.9) (p < 0.0001). Polymorphic amino acids at positions 84 and 11 were associated with CBD: DD versus GG, 2.8 (1.8-4.6), p < 0.0001; GD versus GG, 2.1 (1.5-2.8), p < 0.0001; LL versus GG, 3.2 (1.8-5.6), p < 0.0001; GL versus GG, 2.8 (2.1-3.8), p < 0.0001. Similar results were found within the BeS group and CBD/BeS combined group. We conclude that the less frequent E69 alleles confer more risk for CBD than does *0201. Recent studies examining how the composition and structure of the binding pockets influence peptide binding in MHC genes, as well of studies showing the topology of the TCR to likely bind DPB1 preferentially, give plausible biological rationale for these findings.
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