T-cell receptor Vβ gene segment expression in diisocyanate-induced occupational asthma☆,☆☆,★,★★
Section snippets
Subject population
The diagnosis of DOA was based on history of diisocyanate exposure in the workplace, clinical symptoms that decreased away from work, and peak flow variability at work compared with away from work. The diagnosis of DOA was confirmed by either a workplace or laboratory challenge with diisocyanates. Workers with DOA were further characterized by whether they produced diisocyanate-specific IgE and/or IgG antibodies by using a standardized ELISA method described by Sarlo et al.11 An increased level
PBMC proliferation
The mean proliferative response ranged between 100 and 300 cpm for the HSA control and 50,000 and 100,000 cpm for mitogen (PHA). The maximal proliferative response was observed on day 4 for mitogen and on day 7 for antigen (HDI-HSA, TDI-HSA, or MDI-HSA). The mean proliferative response of PBMCs obtained from workers with DOA (n = 8) stimulated with HDI-HSA and MDI-HSA was significantly greater than the mean proliferative response of PBMCs obtained from diisocyanate-exposed and unexposed control
Discussion
Previous investigations of DOA have attempted to identify specific biomarkers that could be used to detect workers at risk for developing occupational asthma. Diisocyanate-specific IgG antibodies have been previously reported to represent a marker of exposure to diisocyanates, but neither IgG nor IgE antibodies have correlated well with disease activity.26 Similarly, use of PBMC proliferation as a biomarker for identifying workers at risk for DOA appears to be nonspecific for disease activity.2
Acknowledgements
We thank Shervin Yermian and Lynn Whitacre for their contributions to this project.
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Cited by (56)
HLA and asthma phenotypes/endotypes: A review
2014, Human ImmunologyCitation Excerpt :Conversely, allele DQB1*05:01 and the DQA1*01:01-DQB1*05:01-DR1 haplotype was suggested as protective against the disease. Other groups of studies were unable to demonstrate the influence of HLA Class II Alleles in Isocyanate-Induced Asthma, based on a German population [106] and on diisocyanate-exposed workers [107]. Beghé et al. also failed to demonstrate that HLA class I alleles were significantly associated with the phenotype of TDI-induced asthma in a European study [108].
Antigenic changes in human albumin caused by reactivity with the occupational allergen diphenylmethane diisocyanate
2010, Analytical BiochemistryOccupational asthma: Current concepts in pathogenesis, diagnosis, and management
2009, Journal of Allergy and Clinical ImmunologyCitation Excerpt :In white subjects in Northern Italy, it has been reported that there was a significant positive association between TDI-induced OA with HLA- DQA1∗0104 and DQB1∗0503, and a protective association between disease and HLA- DQA1∗0101 and DQB1∗0501.40 However, studies in Germany and the United States were unable to find similar associations.41,42 In a Korean population, a significant association was found between TDI-OA and the DRB1∗15-DPB1∗05 haplotype.43
Epidemiology and aetiological agents of occupational asthma
2007, Archives des Maladies Professionnelles et de l'EnvironnementEpidemiology and aetiological agents of occupational asthma
2006, Revue des Maladies RespiratoiresHuman γ/δT-cell proliferation and IFN-γ production induced by hexamethylene diisocyanate
2003, Journal of Allergy and Clinical Immunology
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From the Divisions of aImmunology, bNephrology, and cPulmonary and Critical Care Medicine; ethe Department of Internal Medicine, Hoxworth Blood Center; and fthe Departments of Environmental Health and Molecular and Cellular Physiology, University of Cincinnati College of Medicine.
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Supported by National Institutes of Health grants NIEHS-ES06096, NIEHS-ES06562, and NIEHS-ES06677 and by the Center for Indoor Air Research (93-08).
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Reprint requests: Jonathan A. Bernstein, MD, College of Medicine, University of Cincinnati, P.O. Box 670563, Cincinnati, OH 45267-0563.
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