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The aryl hydrocarbon receptor in immunity.
Charlotte Esser1, Agneta Rannug, Brigitta Stockinger
1Institut für Umweltmedizinische Forschung, Auf'm Hennekamp 50, 40225 Düsseldorf, Germany. chesser@uni-duesseldorf.de
Trends in Immunology
|August 25, 2009
Summary
Low-molecular-weight chemicals influence immune responses by activating the aryl hydrocarbon receptor (AhR). This review explores AhR
Area of Science:
- Immunology
- Toxicology
- Molecular Biology
Background:
- Emerging evidence suggests low-molecular-weight chemicals (xenobiotics) may contribute to rising allergy and autoimmunity rates.
- The cytosolic transcription factor aryl hydrocarbon receptor (AhR) is a key mediator of immune responses to xenobiotics.
- AhR recognizes diverse molecules, including environmental toxins like dioxin and endogenous compounds.
Purpose of the Study:
- To review the physiological role of the aryl hydrocarbon receptor (AhR) in the immune system.
- To focus on the specific involvement of AhR in T-cell biology and immune regulation.
- To highlight the impact of xenobiotics on immune homeostasis via AhR signaling.
Main Methods:
- Literature review of existing studies on AhR function in immunology.
- Analysis of research on AhR expression in immune cells, particularly Th17 cells and dendritic cells.
- Examination of knockout studies investigating AhR's role in normal physiology and immune responses.
Main Results:
- AhR plays a significant role in normal physiological immune responses, beyond its known role in dioxin toxicity.
- High expression of AhR is observed in critical immune cells like T helper 17 (Th17) cells and dendritic cells.
- Xenobiotic activation of AhR can modulate immune cell function and potentially influence immune-related diseases.
Conclusions:
- The aryl hydrocarbon receptor (AhR) is a crucial regulator of immune system function.
- Understanding AhR's role in T-cell biology is essential for comprehending immune responses to environmental factors.
- Targeting AhR signaling may offer therapeutic strategies for allergies and autoimmune diseases.
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