Aryl hydrocarbon receptor controls murine mast cell homeostasis.
Blood, 2013/4/18;121(16):3195-204.
Zhou Y[1], Tung HY, Tsai YM, Hsu SC, Chang HW, Kawasaki H, Tseng HC, Plunkett B, Gao P, Hung CH, Vonakis BM, Huang SK
Affiliations
PMID: 23462117DOI: 10.1182/blood-2012-08-453597
Impact factor: 25.476
Abstract
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.
MeSH terms
Animals; Antigens; Apoptosis; Calcium; Carbazoles; Cell Degranulation; Cells, Cultured; Gene Deletion; Homeostasis; Humans; Immunoglobulin E; Mast Cells; Mice; Mitochondria; Oxidation-Reduction; Protein Tyrosine Phosphatase, Non-Receptor Type 11; Reactive Oxygen Species; Receptors, Aryl Hydrocarbon; Signal Transduction
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