Journal
CLINICAL IMMUNOLOGY
Volume 121, Issue 2, Pages 134-143Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2006.03.012
Keywords
T cells; beryllium; lung; MHC; genetic susceptibility
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Funding
- NCRR NIH HHS [M01-RR-0051] Funding Source: Medline
- NHLBI NIH HHS [HL62410, R01 HL062410] Funding Source: Medline
- NIEHS NIH HHS [ES11810] Funding Source: Medline
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Chronic beryllium disease (CBD) is a granulomatous lung disorder caused by beryllium exposure in the workplace and is characterized by the accumulation of beryllium-specific CD4(+) T cells. Depending on genetic susceptibility and the nature of the exposure, CBD occurs in up to 20% of exposed workers. Genetic susceptibility has been associated with particular HLA-DP alleles, especially those possessing a negatively charged glutamic acid residue at the 69th position of the p-chain. The mechanism for this association ties in the ability of these HLA-DP molecules to bind and present beryllium to pathogenic CD4(+) T cells. Large numbers of effector memory, beryllium-specific CD4(+) T cells are recruited to the lung of these subjects and secrete Th1-type cytokines upon beryllium recognition. The presence of circulating beryllium-specific CD4(+) T cells directly correlates with the severity of lymphocytic alveolitis. With the presence of a known antigenic stimulus, CBD serves as an important model of immune-mediated, organ destruction. Thus, our findings in CBD have important implications for studies in autoimmune diseases, in particular those with an unknown inciting antigen and an inaccessible target organ. (c) 2006 Elsevier Inc. All rights reserved.
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