Conflicts of interest: None.
Genetic endowment of proinflammatory cytokine tumor necrosis factor-α (–) 308 G > A polymorphism to Parthenium hysterophorus-induced airborne contact dermatitis in an Indian cohort
Article first published online: 14 FEB 2014
© 2014 The International Society of Dermatology
International Journal of Dermatology
How to Cite
Khatri, R., Akhtar, N., Mukhopadhyay, K., Verma, K. K., Sethuraman, G. and Sharma, A. (2014), Genetic endowment of proinflammatory cytokine tumor necrosis factor-α (–) 308 G > A polymorphism to Parthenium hysterophorus-induced airborne contact dermatitis in an Indian cohort. International Journal of Dermatology. doi: 10.1111/ijd.12255
- Article first published online: 14 FEB 2014
- Indian Council of Medical Research
Parthenium dermatitis is a common airborne allergic health problem that induces a cell-mediated hypersensitivity immune response involving activated T lymphocytes, which culminates in injury to the skin. The disease is manifested as itchy erythematous papules and plaques and primarily affects the exposed areas and flexures. This study aimed to identify the role of tumor necrosis factor (TNF)-α (−) 308 G>A polymorphism in the pathogenesis of parthenium dermatitis.
Materials and methods
A total of 120 subjects, including 60 patients exclusively diagnosed for parthenium dermatitis and 60 healthy individuals, were included in the study. The genotyping of the TNF-α (−) 308 G>A region was carried out by the amplification refractory mutational system.
In the present study, we demonstrated that polymorphism of the TNF-α (–) 308 position (A and/or G) was not statistically significant, and there was no difference in the distribution of any alleles of this locus in cases and controls.
The present study suggests that there is a lack of association of potent proinflammatory cytokine TNF-α (−) 308 G>A polymorphism in parthenium dermatitis in the Indian cohort. It interprets genetically endowed transcriptional capacity due to this particular single nucleotide polymorphism but does not support the prevalence of high serum levels of TNF-α in parthenium-induced skin allergic inflammation.