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A Comparison of Mediators Released or Generated by IFN--Treated Human Mast Cells Following Aggregation of FcRI or FcRI¹

Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892

The high affinity receptor for IgG (FcRI, CD64) is expressed on human mast cells, where it is up-regulated by IFN- and, thus, may allow mast cells to be recruited through IgG-dependent mechanisms in IFN--rich tissue inflammation. However, the mediators produced by human mast cells after aggregation of FcRI are incompletely described, and it is unknown whether these mediators are distinct from those produced after activation of human mast cells via FcRI. Thus, we investigated the release of histamine and arachidonic acid metabolites and examined the chemokine and cytokine mRNA profiles of IFN--treated cultured human mast cells after FcRI or FcRI aggregation. Aggregation of FcRI resulted in histamine release and PGD₂ and LTC₄ generation. These responses were qualitatively indistinguishable from responses stimulated via FcRI. Aggregation of FcRI or FcRI led to an induction or accumulation of 22 cytokine and chemokine mRNAs. Among them, seven cytokines (TNF-, IL-1, IL-5, IL-6, IL-13, IL-1R antagonist, and GM-CSF) were significantly up-regulated via aggregation of FcRI compared with FcRI. TNF- mRNA data were confirmed by quantitative RT-PCR and ELISA. Furthermore, we confirmed histamine and TNF- data using IFN--treated purified human lung mast cells. Thus, aggregation of FcRI on mast cells led to up-regulation and/or release of three important classes of mediators: biogenic amines, lipid mediators, and cytokines. Some cytokines, such as TNF-, were released and generated to a greater degree after FcRI aggregation, suggesting that selected biologic responses of mast cells may be preferentially generated through FcRI in an IFN--rich environment.

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