Bernstein JA, Munson J, Lummus ZL, Balakrishnan K, Leikauf G, T-cell receptor V beta gene segment expression in di-isocyanate-induced occupational asthma, J Allergy Clin Immunol, 1997;99:245-250,

BOHRF Original Authors' Main Conclusions

The original authors' main conclusions are taken from Abstract, Results and Discussion. They are decided upon by the authors of the BOHRF occupational asthma guidelines and form part of the guidelines.

Di-isocyanates are the most common cause of occupational asthma induced by low-molecular-weight chemicals. The disease appears to be immunologically mediated but is independent of IgE antibody synthesis. An underlying genetic susceptibility is suggested by the fact that the disease only develops in approximately 5-10% of exposed workers. Study aimed to determine whether disease susceptibility is influenced by HLA and T-cell receptor V beta gene segment usage. Lymphocytes from workers with di-isocyanate-induced occupational asthma had significantly decreased V beta 1 and V beta 5 gene segment expression before in vitro exposure to di-isocyanates, compared with control groups. Percent V beta 1 and V beta 5 gene segment expression was selectively increased when peripheral blood mononuclear cells were stimulated in vitro with di-isocyanate-conjugated proteins. Low-resolution HLA class II phenotyping revealed no significant differences in the distribution of HLA-DR or HLA-DQ alleles between di-isocyanate-induced occupational asthma and control groups. These findings are consistent with a hypothesis that antigen-specific T-cell subpopulations may be sequestered in the lungs of workers with di-isocyanate-induced occupational asthma and clonally expand after further exposure to di-isocyanates.

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