Table I.

Outstanding questions to be addressed in future

1.	Why high concentrations of IgE are required for mast cell survival and activation?
2.	More definitive evidence for receptor aggregation by monomeric IgE should be obtained.
3.	What is the mechanism for receptor aggregation? Is the same mechanism used by monomeric IgE and IgE+Ag to induce receptor aggregation? Does p28 play any role?
4.	What receptor components and parts thereof are required for monomeric IgE-induced receptor up-regulation, survival, cytokine production, and other activation events? Are coreceptor or costimulatory receptors present?
5.	Are the same sets of signaling pathways used by monomeric IgE and IgE+Ag to cause survival, cytokine production, and other activation events?
6.	What makes the difference between HC and PC IgEs? Is there a wide spectrum in the ability of human IgEs similar to that of mouse monoclonal IgEs from HC to PC IgEs. If so, do such differences in human IgEs have pathophysiological significance? Do allergic patients tend to have HC IgEs than nonallergic individuals?