Journal
BLOOD
Volume 121, Issue 16, Pages 3195-3204Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2012-08-453597
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Funding
- National Institutes of Health [AI052468, AI073610]
- National Health Research Institutes of Taiwan [EOPP10-014, EOSP07-014]
- National Science Council of Taiwan [NSC 100-3114-Y-043-002/00D1-EODOH01]
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We propose that the aryl hydrocarbon receptor (AhR), a unique chemical sensor, is critical in controlling mast cell differentiation, growth, and function in vitro and in vivo. In antigen-stimulated mast cells, exposure to AhR ligands resulted in a calcium-and reactive oxygen species (ROS)-dependent increase of reversible oxidation in and reduced activity of SHP-2 phosphatase, leading to enhanced mast cell signaling, degranulation, and mediator and cytokine release, as well as the in vivo anaphylactic response. Surprisingly, significant mast cell deficiency was noted in AhR-null mice due to defective calcium signaling and mitochondrial function, concomitant with reduced expression of c-kit and cytosolic STAT proteins, as well as enhanced intracellular ROS and apoptosis. Consequently, AhR-null mast cells responded poorly to stimulation, demonstrating a critical role of AhR signaling in maintaining mast cell homeostasis.
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