ReviewJournal of immunology (Baltimore, Md. : 1950)2016
Beryllium-Induced Hypersensitivity: Genetic Susceptibility and Neoantigen Generation.
Review in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 56 citations in OpenAlex.
- Reduced CCL/Be-specific CD4+ T cells in CCL3-deficient or peptide-MHCII CAR-T cell-treated mice.JCI insight · 2026Article
- Adverse local tissue reactions in arthroplasty: opportunities and challenges for a common terminology across scientific, clinical and regulatory fields.EFORT open reviews · 2025Article
- Interleukin-1 signaling and CD4Frontiers in immunology · 2025Article
- Review
- Protective role of tissue-resident Tregs in a murine model of beryllium-induced disease.JCI insight · 2022Article
- [Sarcoidosis and berylliosis].Der Internist · 2022Review
- Beryllium-specific CD4+ T cells induced by chemokine neoantigens perpetuate inflammation.The Journal of clinical investigation · 2021Article
- Pulmonary Macrophage Cell Death in Lung Health and Disease.American journal of respiratory cell and molecular biology · 2021Review
- Analysis of single nucleotide polymorphisms in chronic beryllium disease.Respiratory research · 2021Article
- Replication of HLA class II locus association with susceptibility to podoconiosis in three Ethiopian ethnic groups.Scientific reports · 2021Article
- 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
- Metal Imbalance in Neurodegenerative Diseases with a Specific Concern to the Brain of Multiple Sclerosis Patients.International journal of molecular sciences · 2020Review
- Environmental Risk Factors for Sarcoidosis.Frontiers in immunology · 2020Review
- Current Sarcoidosis Models and the Importance of Focusing on the Granuloma.Frontiers in immunology · 2020Review
- Metal-triggered conformational reorientation of a self-peptide bound to a disease-associated HLA-B*27 subtype.The Journal of biological chemistry · 2019Article
- Translational research in pulmonary fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Protective role of B cells in sterile particulate-induced lung injury.JCI insight · 2019Article
- Mechanisms of Adverse Local Tissue Reactions to Hip Implants.Frontiers in bioengineering and biotechnology · 2019Review
- Hide and Seek: Nanomaterial Interactions With the Immune System.Frontiers in immunology · 2019Review
- TLR9 and IL-1R1 Promote Mobilization of Pulmonary Dendritic Cells during Beryllium Sensitization.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic beryllium (Be) disease is a granulomatous lung disorder that results from Be exposure in a genetically susceptible host. The disease is characterized by the accumulation of Be-responsive CD4(+) T cells in the lung, and genetic susceptibility is primarily linked to HLA-DPB1 alleles possessing a glutamic acid at position 69 of the β-chain. Recent structural analysis of a Be-specific TCR interacting with a Be-loaded HLA-DP2-peptide complex revealed that Be is coordinated by amino acid residues derived from the HLA-DP2 β-chain and peptide and showed that the TCR does not directly interact with the Be(2+) cation. Rather, the TCR recognizes a modified HLA-DP2-peptide complex with charge and conformational changes. Collectively, these findings provide a structural basis for the development of this occupational lung disease through the ability of Be to induce posttranslational modifications in preexisting HLA-DP2-peptide complexes, resulting in the creation of neoantigens.
Indexed as
Identifiers
What OpenQuestion holds
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.