Apoptosis of mouse mast cells is reciprocally regulated by the IgG receptors FcγRIIB and FcγRIIIA

Authors

  • Y. Fang,

    1. Department of Microbiology and Immunology, Affiliated Hospital of Guiyang Medical College, Guiyang, China
    2. Department of Microbiology and Immunology, Mucosal Immunobiology and Vaccine Research Center, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden
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    • These authors contributed equally.
  • L. Larsson,

    1. Department of Microbiology and Immunology, Mucosal Immunobiology and Vaccine Research Center, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden
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    • These authors contributed equally.
  • P. Bruhns,

    1. Institut Pasteur, Unité d'Allergologie Moléculaire et Cellulaire, Département d'Immunologie, Paris, France
    2. INSERM, Paris, France
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  • Z. Xiang

    Corresponding author
    1. Department of Microbiology and Immunology, Mucosal Immunobiology and Vaccine Research Center, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden
    • Department of Microbiology and Immunology, Affiliated Hospital of Guiyang Medical College, Guiyang, China
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  • Edited by: Hans-Uwe Simon

Correspondence

Zou Xiang, Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Gothenburg 405 30, Sweden.

Tel.: +46 31 7866322

Fax: +46 31 7866330

E-mail: zou.xiang@gu.se

Abstract

Background

Mast cells are important effector cells in allergy. They usually have a long life span and resist cell death induction. Fcγ receptor– and IgG immune complex–mediated apoptosis has been demonstrated in B-lineage cells, but not in mast cells. The aim of the current study was to investigate whether mast cells could respond to apoptosis induction by IgG immune complex aggregation of Fcγ receptors. It is known that mouse mast cells express the low-affinity Fcγ receptors FcγRIIB and FcγRIIIA, which bind IgG especially in the form of antigen–IgG immune complexes.

Methods

Mouse bone marrow–derived cultured mast cells were examined for surface expression of FcγRIIB and FcγRIIIA. Apoptosis of such cells from wild-type, FcγRIIB−/− or FcγRIIIA−/− mice was measured following receptor aggregation by IgG immune complexes.

Results

Our data demonstrate that aggregation of either FcγRIIB or FcγRIIIA by IgG immune complexes induced apoptosis of mouse bone marrow–derived cultured mast cells. However, mast cells expressing both FcγRIIB and FcγRIIIA were able to resist cell death induction by IgG immune complexes.

Conclusion

Our findings reveal a fine-tuning system for regulating mast cell apoptosis through aggregating Fcγ receptors by IgG immune complexes. Such apoptosis regulation may have a substantial impact on mast cell homeostasis during allergic inflammation.

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