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Abstract
The aryl hydrocarbon receptor is a ligand-activated transcriptional regulator that binds dioxin and other exogenous contaminants and is responsible for their toxic effects, including immunosuppression. New evidence suggests, however, that the aryl hydrocarbon receptor has a physiological role in the immune system, and the immunosuppressive effects of dioxin may reflect a more subtle disruption of the regulatory interactions between immune cells.
Highlights
aryl hydrocarbon receptor (AhR) is conserved across vertebrate and invertebrate species, playing a role, for instance, in the development of the nervous system in Caenorhabditis elegans, while in Drosophila the AhR homolog spineless is involved in development of antennae and legs as well as in aspects of color vision [1].The intrinsic physiological functions of AhR in mammals have been delineated from the phenotype of the AhR knockout mouse [2,3,4]
More recently it has been suggested that dioxin-mediated toxicity may, reflect disruption of the endogenous function of this receptor by inducing sustained and inappropriate AhR signaling due to the stability of the toxin, and causing dysregulation of physiological functions [5]
Toxic effects of dysregulation are likely in the immune system where highly complex interactions between hematopoietic cells and their environment dictate the outcome of challenge by pathogens, and dioxin has been known for decades to be immunotoxic, though information on possible underlying mechanisms is sparse [6]
Summary
AhR is conserved across vertebrate and invertebrate species, playing a role, for instance, in the development of the nervous system in Caenorhabditis elegans, while in Drosophila the AhR homolog spineless is involved in development of antennae and legs as well as in aspects of color vision [1].The intrinsic physiological functions of AhR in mammals have been delineated from the phenotype of the AhR knockout mouse [2,3,4]. CD4 T cells are further subdivided into four clearly defined subsets with distinct functions that are mediated by the distinct cytokines they secrete and that act on other immune cells (Figure 1), including B cells, which they activate to secrete antibody.
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