ArticleMucosal immunology2016
Metal-specific CD4+ T-cell responses induced by beryllium exposure in HLA-DP2 transgenic mice.
Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Protective role of tissue-resident Tregs in a murine model of beryllium-induced disease.JCI insight · 2022Article
- Innate and Adaptive Immunity in Noninfectious Granulomatous Lung Disease.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- Generation and expression analysis of BAC humanized mice carrying HLA-DP401 haplotype.Animal models and experimental medicine · 2021Article
- Beryllium-specific CD4+ T cells induced by chemokine neoantigens perpetuate inflammation.The Journal of clinical investigation · 2021Article
- Protective role of B cells in sterile particulate-induced lung injury.JCI insight · 2019Article
- TLR9 and IL-1R1 Promote Mobilization of Pulmonary Dendritic Cells during Beryllium Sensitization.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Genetic, Immunologic, and Environmental Basis of Sarcoidosis.Annals of the American Thoracic Society · 2017Review
- The role of HLA genes in pharmacogenomics: unravelling HLA associated adverse drug reactions.Immunogenetics · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic beryllium disease (CBD) is a granulomatous lung disorder that is associated with the accumulation of beryllium (Be)-specific CD4(+) T cells into the lung. Genetic susceptibility is linked to HLA-DPB1 alleles that possess a glutamic acid at position 69 (βGlu69), and HLA-DPB1*02:01 is the most prevalent βGlu69-containing allele. Using HLA-DP2 transgenic (Tg) mice, we developed a model of CBD that replicates the major features of the human disease. Here we characterized the T-cell receptor (TCR) repertoire of Be-responsive CD4(+) T cells derived from the lungs of Be oxide-exposed HLA-DP2 Tg mice. The majority of Be-specific T-cell hybridomas expressed TCR Vβ6, and a subset of these hybridomas expressed identical or nearly identical β-chains that were paired with different α-chains. We delineated mimotopes that bind to HLA-DP2 and form a complex recognized by Be-specific CD4(+) T cells in the absence of Be. These Be-independent peptides possess an arginine at p5 and a tryptophan at p7 that surround the Be-binding site within the HLA-DP2 acidic pocket and likely induce charge and conformational changes that mimic those induced by the Be(2+) cation. Collectively, these data highlight the interplay between peptides and Be in the generation of an adaptive immune response in metal-induced hypersensitivity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.