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*
Department of Immunology, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom;
Department of Cell Biology and Development, University "La Sapienza", Rome, Italy;
Royal Brompton Hospital, London, United Kingdom;
Department of Medicine, University of Wales College of Medicine, Cardiff, United Kingdom; and
¶ Division of Respiratory Diseases of the University of "Tor Vergata" at the L. Spallanzani Hospital, Institute for Research and Clinical Care, Rome, Italy
Occupational exposure to small molecules, such as metals, is
frequently associated with hypersensitivity reactions. Chronic
beryllium (Be) disease (CBD) is a multisystem granulomatous disease
that primarily affects the lung, and occurs in 
3% of individuals
exposed to this element. Immunogenetic studies have demonstrated a
strong association between CBD and possession of alleles of HLA-DP
containing glutamic acid (Glu) at position 69 in the HLA-DP
-chain. T
cell clones were raised from three patients with CBD in whom exposure
occurred 10 and 30 years previously. Of 25 Be-specific clones that were
obtained, all were restricted by HLA-DP alleles with Glu at DP69.
Furthermore, the proliferative responses of the clones were absolutely
dependent upon DP Glu69 in that a single amino acid
substitution at this position abolished the response. As befits a
disease whose pathogenesis involves a delayed type hypersensitivity
response, the large majority of Be-specific clones secreted IFN-
(Th1) and little or no IL-4 (Th2) cytokines. This study provides
insights into the molecular basis of DP2-associated susceptibility to
CBD.
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