期刊
JOURNAL OF IMMUNOLOGY
卷 196, 期 1, 页码 22-27出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1502011
关键词
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类别
资金
- National Institutes of Health [HL62410, HL92997, ES011810, ES25797]
- Clinical and Translational Sciences Institute from the National Center for Advancing Translational Sciences) [UL1 TR000154]
- Boettcher Foundation
- American Thoracic Society
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 b-chain. Recent structural analysis of a Be-specific TCR interacting with a Be-loaded HLADP-2-peptide complex revealed that Be is coordinated by amino acid residues derived from the HLA-DP2 b-chain and peptide and showed that the TCR does not directly interact with the Be2+ 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.
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