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FcRIIa, Not FcRIIb, Is Constitutively and Functionally Expressed on Skin-Derived Human Mast Cells¹

Wei Zhao^2,*, Christopher L. Kepley^2,, Penelope A. Morel, Lawrence M. Okumoto^*, Yoshihiro Fukuoka and Lawrence B. Schwartz^3,

Departments of ^* Pediatrics and Internal Medicine, Virginia Commonwealth University, Richmond, VA 23298; and Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15213

The expression of FcR by human skin-derived mast cells of the MC_TC type was determined in the current study. Expression of mRNA was analyzed with microarray gene chips and RT-PCR; protein by Western blotting and flow cytometry; function by release of -hexosaminidase, PGD₂, leukotriene C₄ (LTC₄), IL-5, IL-6, IL-13, GM-CSF, and TNF-. FcRIIa was consistently detected along with FcRI at the mRNA and protein levels; FcRIIc was sometimes detected only by RT-PCR; but FcRIIb, FcRI, and FcRIII mRNA and protein were not detected. FcRIIa-specific mAb caused skin MC_TC cells to degranulate and secrete PGD₂, LTC₄, GM-CSF, IL-5, IL-6, IL-13, and TNF- in a dose-dependent fashion. FcRI-specific mAb caused similar amounts of each mediator to be released with the exception of LTC₄, which was not released by this agonist. Simultaneous but independent cross-linking of FcRI and FcRIIa did not substantially alter mediator release above or below levels observed with each agent alone. Skin MC_TC cells sensitized with dust-mite-specific IgE and IgG, when coaggregated by Der p2, exhibited enhanced degranulation compared with sensitization with either IgE or IgG alone. These results extend the known capabilities of human skin mast cells to respond to IgG as well as IgE-mediated signals.

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