Activation of human mast cells through the high affinity IgG receptor.

Mast cells are known to participate in the induction of inflammation through interaction of antigen with specific IgE bound to the high affinity receptor for IgE (FcepsilonRI). Human mast cells, derived from CD34(+) hematopoietic precursors, not only express FcepsilonRI but also express high affinity receptors for IgG (FcgammaRI), the latter only after IFN-gamma exposure. Human mast cells that express FcgammaRI are activated following FcgammaRI aggregation, either using antibodies directed to the receptor or through IgG bound to the receptor. This activation results in degranulation, with the release of granule-associated mediators, and the generation of metabolites of arachidonic acid and secretion of chemokines and cytokines. These observations provide evidence that human mast cells may also be recruited into inflammation through IgG-dependent mechanisms.