IL-4 selectively enhances FcgRIII expression and signaling on mouse mast cells

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Christopher Kepley, Associate Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
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Abstract: Fc receptors for IgG (Fc?R) are widely expressed in the hematopoietic system and mediate a variety of inflammatory responses. There are two functional classes of FcgR, activation and inhibitory receptors. Since IgG immune complexes (IgG IC) bind each class with similar affinity, co-expression of these receptors leads to their co-ligation. Thus, expression levels of this antagonistic pair play a critical role in determining the cellular response. Murine mast cells co-express the activation receptor FcgRIII and the inhibitory receptor FcgRIIb and can be activated by IgG IC. Mast cell activation contributes to allergic and other inflammatory diseases—particularly those in which IgG IC may play important roles. Using mouse bone marrow-derived mast cells, we report that IL-4 selectively increases FcgRIII expression without altering FcgRIIb. This enhanced expression could be induced by Stat6 activation alone, and appeared to be mediated in part by increased FcgRIIIa protein synthesis without significant changes in transcription. The increase in FcgRIII expression was functionally significant, as it was matched by enhanced FcgR-mediated degranulation and cytokine production. Selective regulation of mast cell FcgR by interleukin-4 could alter inflammatory IgG responses and subsequently disease severity and progression.

Additional Information

Cellular Immunology 2003; 224(2):65-73.
Language: English
Date: 2003
Mast cell, FcgR, IL-4, CD16

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