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Lack of association of HLA class I genes and TNF α ‐308 polymorphism in toluene diisocyanate‐induced asthma
Author(s) -
Beghé B.,
Padoan M.,
Moss C. T.,
Barton S. J.,
Holloway J. W.,
Holgate S. T.,
Howell W. M.,
Mapp C. E.
Publication year - 2004
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1046/j.1398-9995.2003.00352.x
Subject(s) - toluene diisocyanate , asthma , immunology , asymptomatic , human leukocyte antigen , gene polymorphism , tumor necrosis factor alpha , antigen , medicine , genetic predisposition , allele , gene , biology , chemistry , genetics , pathology , organic chemistry , polyurethane
Background: Toluene diisocyanate (TDI)‐induced asthma is a common cause of occupational asthma and it affects 5–15% of the exposed population suggesting an underlying genetic susceptibility. Methods: To investigate the role of genetic factors in the development of TDI‐induced asthma, we analyzed the distribution of human leukocyte antigen (HLA) class I genes and of tumor necrosis factor (TNF)‐ α A‐308G polymorphism in 142 patients with TDI‐induced asthma and in 50 asymptomatic exposed subjects. Results: Neither the distribution of HLA class I antigens nor the distribution of TNF‐ α A‐308G polymorphism was different between patients with TDI‐induced asthma and asymptomatic exposed subjects. Conclusions: These results suggest that HLA class I antigens and TNF‐ α A‐308G are not associated with susceptibility or resistance to the development of TDI‐induced asthma.