The Role of the Aryl Hydrocarbon Receptor (AHR) in Immune and Inflammatory Diseases

The aryl hydrocarbon receptor (AHR) is a nuclear receptor that modulates the response to environmental stimuli. It was recognized historically for its role in toxicology but, in recent decades, it has been increasingly recognized as an important modulator of disease-especially for its role in modula...

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Vydané v:International journal of molecular sciences Ročník 19; číslo 12; s. 3851
Hlavní autori: Neavin, Drew R, Liu, Duan, Ray, Balmiki, Weinshilboum, Richard M
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Switzerland MDPI AG 03.12.2018
MDPI
Predmet:
Cell culture
Congenital diseases
Cytochrome
Cytokines
Disease
Drug dosages
Enzymes
Gene expression
Herpes viruses
Hydrocarbons
Infections
Ligands
Metabolism
Multiple sclerosis
Nervous system
Pathogenesis
Pathogens
Review
Sepsis
Tumor necrosis factor-TNF
aryl hydrocarbon receptor (AHR)
tryptophan (TRP)
single nucleotide polymorphisms (SNPs)
aryl hydrocarbon response element (AHRE)
ISSN:1661-6596, 1422-0067, 1422-0067
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Popis
Shrnutí:The aryl hydrocarbon receptor (AHR) is a nuclear receptor that modulates the response to environmental stimuli. It was recognized historically for its role in toxicology but, in recent decades, it has been increasingly recognized as an important modulator of disease-especially for its role in modulating immune and inflammatory responses. AHR has been implicated in many diseases that are driven by immune/inflammatory processes, including major depressive disorder, multiple sclerosis, rheumatoid arthritis, asthma, and allergic responses, among others. The mechanisms by which AHR has been suggested to impact immune/inflammatory diseases include targeted gene expression and altered immune differentiation. It has been suggested that single nucleotide polymorphisms (SNPs) that are near AHR-regulated genes may contribute to AHR-dependent disease mechanisms/pathways. Further, we have found that SNPs that are outside of nuclear receptor binding sites (i.e., outside of AHR response elements (AHREs)) may contribute to AHR-dependent gene regulation in a SNP- and ligand-dependent manner. This review will discuss the evidence and mechanisms of AHR contributions to immune/inflammatory diseases and will consider the possibility that SNPs that are outside of AHR binding sites might contribute to AHR ligand-dependent inter-individual variation in disease pathophysiology and response to pharmacotherapeutics.
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Present affiliation: Assurex Health Inc., Mason, OH 45040, USA.
ISSN:1661-6596
1422-0067
1422-0067
DOI:10.3390/ijms19123851