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Review

Genetic variants affecting chemical mediated skin immunotoxicity

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ABSTRACT

The skin is an immune-competent organ and this function may be impaired by exposure to chemicals, which may ultimately result in immune-mediated dermal disorders. Interindividual variability to chemical-induced skin immune reactions is associated with intrinsic individual characteristics and their genomes. In the last 30–40 years, several genes influencing susceptibility to skin immune reactions were identified. The aim of this review is to provide information regarding common genetic variations affecting skin immunotoxicity. The polymorphisms selected for this review are related to xenobiotic-metabolizing enzymes (CYPA1 and CYPB1 genes), antioxidant defense (GSTM1, GSTT1, and GSTP1 genes), aryl hydrocarbon receptor signaling pathway (AHR and ARNT genes), skin barrier function transepidermal water loss (FLG, CASP14, and SPINK5 genes), inflammation (TNF, IL10, IL6, IL18, IL31, and TSLP genes), major histocompatibility complex (MHC) and neuroendocrine system peptides (CALCA, TRPV1, ACE genes). These genes present variants associated with skin immune responses and diseases, as well as variants associated with protecting skin immune homeostasis following chemical exposure. The molecular and association studies focusing on these genetic variants may elucidate their functional consequences and contribution in the susceptibility to skin immunotoxicity. Providing information on how genetic variations affect the skin immune system may reduce uncertainties in estimating chemical hazards/risks for human health in the future.

Acknowledgments

Thanks are due to National Council for Scientific and Technological Development (CNPq: 465571/2014-0) and Coordination for the Improvement of Higher Education Personnel - Brazil (CAPES: Financing Code 001).

Disclosure statement

No potential conflict of interest was reported by the author(s).

Correction Statement

This article has been republished with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

This work was supported by the National Council for Scientific and Technological Development (CNPq: 465571/2014-0) and Coordination for the Improvement of Higher Education Personnel - Brazil (CAPES: Financing Code 001).

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