Association between HLA genes and susceptibility to toluene diisocyanate‐induced asthma

Mapp, C. E.; Beghè, Bianca; Balboni, A; Zamorani, G.; Padoan, Michele; Jovine, Luca; Baricordi, Olavio R.; Fabbri, Leonardo M.

doi:10.1046/j.1365-2222.2000.00807.x

Cited by 93 publications

(67 citation statements)

References 18 publications

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“…Although results are still preliminary, several human leukocyte antigen (HLA) markers have been identified that appear to be protective, whereas other markers appear to confer increased risk of WRA (42,43).…”

Section: Work-related Asthma: Workforce-based Studiesmentioning

confidence: 99%

Work-related asthma and implications for the general public.

Petsonk

2002

Environ Health Perspect

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Section: Work-related Asthma: Workforce-based Studiesmentioning

confidence: 99%

Work-related asthma and implications for the general public.

Petsonk

2002

Environ Health Perspect

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“…There have been a few HLA association studies in patients with isocyanate-induced asthma. An association of TDI-OA with HLA-DQB1*0503 and an inverse relationship with HLA-DQB1*0501 was found in a European population [17,18,19], whereas no significant HLA association was found in another European study [20]. Recently, we investigated the HLA associations in TDI-OA and found an association between this disease and the DRB1*15-DPB1*05 haplotype in a Korean population, which suggested a susceptible gene marker for TDI-induced asthma [21].…”

Section: Introductionmentioning

confidence: 99%

The HLA DRB11501-DQB10602-DPB1*0501 Haplotype Is a Risk Factor for Toluene Diisocyanate-Induced Occupational Asthma

Choi

Lee

Kim

et al. 2009

Int Arch Allergy Immunol

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Background: Although the pathogenesis of toluene diisocyanate (TDI)-induced occupational asthma (TDI-OA) is incompletely understood, several studies have suggested immunologic mechanisms, including specific IgE responses. A few studies have suggested human leukocyte antigen (HLA) associations with TDI-induced asthma in Western countries, but this is the first investigation of associations between HLA class I and II alleles and TDI-induced asthma patients in Asia, using high-resolution analysis. Methods: Patients with TDI-OA (n = 84), asymptomatic exposed controls (AECs, n = 47) and unexposed normal controls (NCs, n = 127) were enrolled. HLA class I and II genotyping was performed by the direct DNA sequencing analysis. Specific serum IgE antibodies to the vapor type TDI-albumin conjugate were measured by ELISA. Results: There was no significant association between the allele frequencies and the phenotype of TDI-OA. However, the frequency of the HLA DRB1*1501-DQB1*0602-DPB1*0501 haplotype was significantly higher in TDI-OA patients (19%) than in AEC (2.1%, p = 0.007, OR 4.429, CI 1.497–13.103) or NC (3.1%, p < 0.001, OR 7.235, CI 2.236–22.510) subjects, with statistical significance persisting after correction for multiple comparisons. DQB1*0402 was significantly associated with the presence of specific IgE to TDI-albumin conjugates in serum (p = 0.006, OR 4.552, CI 1.540–13.449). This p value remained significant after correction for multiple comparison. Conclusion: The HLA DRB1*1501-DQB1*0602-DPB1*0501 haplotype may be a genetic marker for the development of TDI-induced asthma in Koreans. Several HLA alleles that enhance specific IgE sensitization in exposed subjects are indicated.

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“…Human lymphocyte antigen (HLA) class 2 molecules have a crucial role in the immune response that occurs in occupational asthma. In one study, 67 workers with TDI induced asthma and 27 asymptomatic controls were genotyped for three HLA class 2 genes: DQA1, DQB1, and DRB1 (Mapp et al, 2000). Asthmatics were found to have a significantly higher frequency of specific alleles for DQA1 and DQB1, while controls had higher frequencies of two other alleles for DQA1 and DQB1.…”

Section: Genetic Polymorphismmentioning

confidence: 99%

Occupational Exposure Gene Interaction : Review Article

2013

Egypt. J. Occup. Med.

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The lack of knowledge about the earliest events in occupational disease development is due to the multi-factorial nature of disease risk. This information gap is the consequence of the lack of appreciation for the fact that most occupational diseases arise from the complex interactions between genes and the occupational exposure. Whether an occupational exposure causes illness or not is dependent on the efficiency of metabolic pathways. Thus, elucidating the causes of most chronic diseases will require an understanding of both the genetic and occupational contribution to their etiology. Unfortunately, the exploration of the relationship between genes and the occupational exposure has been hampered in the past by the limited knowledge of the human genome, and by the inclination of scientists to study disease development using experimental models that consider exposure to a single environmental agent in the workplace. To understand how genes and occupational agents interact to initiate biological pathways to cause injury or disease, scientists will need tools with the capacity to monitor the global expression of thousands of genes, proteins and metabolites simultaneously. The generation of such data in multiple species can be used to identify conserved and functionally significant genes and pathways involved in gene environment interactions. The complex interplay between genes and occupational exposure represents also a great challenge to scientists, and it is also an important opportunity to reduce the burden of disease and dysfunctions on humans. Major technological advances in the last few years have increased our knowledge of the role that genetics has in occupational diseases and our understanding of genetic components and the interaction between genetics and environmental factors. The complex interplay between genes and occupational exposure represents also a great challenge to scientists, and it is also an important opportunity to reduce the burden of disease and dysfunctions on humans.

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Association between HLA genes and susceptibility to toluene diisocyanate‐induced asthma

Abstract: The results of this study indicate that HLA-regulated immune mechanisms are involved in TDI-induced asthma and that, in exposed subjects, specific factors may increase or decrease the risk of developing disease.

Cited by 93 publications

References 18 publications

Work-related asthma and implications for the general public.

Work-related asthma and implications for the general public.

The HLA DRB11501-DQB10602-DPB1*0501 Haplotype Is a Risk Factor for Toluene Diisocyanate-Induced Occupational Asthma

Occupational Exposure Gene Interaction : Review Article

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Association between HLA genes and susceptibility to toluene diisocyanate‐induced asthma

Abstract: The results of this study indicate that HLA-regulated immune mechanisms are involved in TDI-induced asthma and that, in exposed subjects, specific factors may increase or decrease the risk of developing disease.

Cited by 93 publications

References 18 publications

Work-related asthma and implications for the general public.

Work-related asthma and implications for the general public.

The HLA DRB1*1501-DQB1*0602-DPB1*0501 Haplotype Is a Risk Factor for Toluene Diisocyanate-Induced Occupational Asthma

Occupational Exposure Gene Interaction : Review Article

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The HLA DRB11501-DQB10602-DPB1*0501 Haplotype Is a Risk Factor for Toluene Diisocyanate-Induced Occupational Asthma