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Influence of FAS on murine mast cell maturation
Beata Berent-Maoz1, Chamutal Gur, Francesca Vita
1Department of Pharmacology and Experimental Therapeutics, Institute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
Background:
FAS has been shown to be involved in the regulation of many immune processes by induction of cellular apoptosis. However, accumulated evidence shows that FAS signaling also exhibits nonapoptotic functions, such as induction of cell proliferation and differentiation. FAS is the only death receptor known to be expressed on murine mast cells (MCs).
Objective:
To evaluate the role of FAS on murine MC maturation.
Methods:
Mouse bone marrow-derived MCs (BMMCs) or peritoneal MCs were derived from FAS-deficient, FASlpr/lpr, and congenic wild-type strains. The MC degranulation and cytokine release after IgE activation was assessed by measuring β-hexosaminidase, interleukin 13, and tumor necrosis factor α release. Transmission electron microscopy analysis was performed to evaluate the level of BMMC maturation. The surface markers and intracellular preformed mediators were measured as well.
Results:
Our data reveal that FAS deficiency has an impact on IgE-dependent activation of BMMCs, resulting in a significant decrease in β-hexosaminidase, interleukin 13, and tumor necrosis factor α release. The total content of preformed mediators (eg, tryptase and β-hexosaminidase) was reduced in BMMCs derived from FAS-deficient mice. We also found that the level of FcεRI in peritoneal mast cells from FAS-deficient mice was significantly diminished. FAS deficiency also influenced the kinetics of BMMC maturation as was revealed by transmission electron microscopy analysis.
Conclusion:
Our data show that FAS has an impact on the regulation of mouse MC maturation in vitro.
Insights
FAS signaling impacts mouse mast cell (MC) maturation. FAS deficiency reduced IgE-dependent MC activation, cytokine release, and mediator content, affecting MC development.
Area of Science:
- Immunology
- Cell Biology
Background:
- FAS receptor plays a role in immune regulation via apoptosis.
- FAS signaling also mediates nonapoptotic functions like proliferation and differentiation.
- FAS is uniquely expressed on murine mast cells (MCs).
Purpose of the Study:
- To investigate the role of FAS in murine MC maturation.
- To understand FAS-mediated regulation of mast cell development.
Main Methods:
- Mast cells were derived from FAS-deficient and wild-type mice.
- Assessed IgE-dependent activation, cytokine release (IL-13, TNF-α), and degranulation (β-hexosaminidase).
- Evaluated MC maturation using transmission electron microscopy and surface marker analysis.
Main Results:
- FAS deficiency significantly decreased IgE-dependent mast cell activation and release of β-hexosaminidase, IL-13, and TNF-α.
- Reduced levels of preformed mediators (tryptase, β-hexosaminidase) and FcεRI were observed in FAS-deficient mast cells.
- FAS deficiency altered the kinetics of mast cell maturation.
Conclusions:
- FAS plays a significant role in regulating mouse mast cell maturation in vitro.
- FAS signaling is crucial for optimal mast cell development and function.
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