Differential uptake of serum IgE in skin and serosal mast cells(139.14)

Abstract

Abstract Background: Mast cells (MC) are key effector cells in helminth infection and the clinical manifestations of allergic disease. In mice, a subset of MC (Connective Tissue MC) resides at epithelial barriers, such as the skin, or at serosal surfaces, including the peritoneal cavity. These MC exert much of their effector function by virtue of IgE binding to the high affinity Fc epsilon receptor (FcεRI ). Objective: Although acquisition of serum immunoglobulin E (IgE) by skin MC is central to MC effector function, the mechanisms that govern loading of IgE on skin MC are poorly defined. We hypothesize that different anatomic compartments may exhibit differential serum IgE uptake. Methods: We used the mouse ear as a source of skin MC. To control the dose and timing of serum IgE, we used a passive, intravenous IgE transfer model with flow cytometric analysis of MC IgE uptake at time points between 1 and 96 hours after infusion. As controls, we examined serum IgE uptake by spleen basophils and peritoneal mast cells (PEC-MC). Results: We observed differences in IgE uptake by basophils and PEC-MC compared to skin MC. Basophils and PEC-MC displayed uniform loading of IgE that started within 1 hour of IgE exposure. By contrast, skin MC IgE uptake was heterogeneous with only 30% of MC showing significant acquisition of IgE. The timing of uptake was slightly delayed, and the amount of IgE on these cells was also diminished compared to basophils and PEC-MC. Conclusion and Future Directions: Our data suggest that skin and serosal MC demonstrate distinct patterns of IgE uptake and that a select population of skin MC acquires serum IgE upon exposure. Further work will focus on direct in vivo imaging of MC IgE loading within ear tissue to better understand the underlying reason for decreased skin MC uptake of serum IgE.