Abstract

Carcinogenicity of dioxins seems to be largely mediated by their binding to the aryl hydrocarbon receptor (AhR), a cytosolic transcriptional regulator of cell growth, differentiation, and migration. The most widely studied agonist of AhR, in the last thirty years, is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which also presents the highest binding affinity for this receptor. The activated ligand-AhR complex has been described to contribute in suppressing both humoral and cellular immune responses. Starting from the description of the main mechanisms underlying the physiological activation of AhR, the present review is aimed at evaluating a putative functional role of the intragenic AhR polymorphisms, which could greatly affect the functionality of the receptor by either inducing or contrasting its ligand-dependent activation. As consequence, this may participate in lowering or increasing the risk of cancer, particularly, in the most polluted areas.

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