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Receptor I Expression and IgE-Dependent Release of Histamine and Lipid Mediators from Human Umbilical Cord Blood-Derived Mast Cells: Synergistic Effect of IL-4 and IgE on Human Mast Cell Fc Receptor I Expression and Mediator Release1
Departments of
*
Pathology and
Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215;
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852; and
§
Department of Immunology, Juntendo University, School of Medicine, Tokyo, Japan
We investigated the effects of IgE versus IL-4 on Fc
RI surface
expression in differentiated human mast cells derived in vitro from
umbilical cord blood mononuclear cells. We found that IgE (at 5
µg/ml) much more strikingly enhanced surface expression of FcRI
than did IL-4 (at 0.1–100 ng/ml); similar results were also obtained
with differentiated mouse mast cells. However, IL-4 acted
synergistically with IgE to enhance FcRI expression in these
umbilical cord blood-derived human mast cells, as well as in mouse
peritoneal mast cells derived from IL-4-/- or
IL-4+/+ mice. We also found that: 1) IgE-dependent
enhancement of FcRI expression was associated with a significantly
enhanced ability of these human mast cells to secrete histamine,
PGD2, and leukotriene C4 upon subsequent
passive sensitization with IgE and challenge with anti-IgE; 2)
preincubation with IL-4 enhanced IgE-dependent mediator secretion in
these cells even in the absence of significant effects on FcRI
surface expression; 3) when used together with IgE, IL-4 enhanced
IgE-dependent mediator secretion in human mast cells to levels greater
than those observed in cells that had been preincubated with IgE alone;
and 4) batches of human mast cells generated in vitro from umbilical
cord blood cells derived from different donors exhibited differences in
the magnitude and pattern of histamine and lipid mediator release in
response to anti-IgE challenge, both under baseline conditions and
after preincubation with IgE and/or IL-4.
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