Monomeric IgE Stimulates Signaling Pathways in Mast Cells that Lead to Cytokine Production and Cell Survival
2001; Cell Press; Volume: 14; Issue: 6 Linguagem: Inglês
10.1016/s1074-7613(01)00159-5
ISSN1097-4180
AutoresJanet Kalesnikoff, Michael Huber, Vivian Lam, Jacqueline E. Damen, Juan Zhang, Reuben P. Siraganian, Gerald Krystal,
Tópico(s)T-cell and B-cell Immunology
ResumoAlthough IgE binding to mast cells is thought to be a passive presensitization step, we demonstrate herein that monomeric IgE (mIgE) in the absence of antigen (Ag) stimulates multiple phosphorylation events in normal murine bone marrow-derived mast cells (BMMCs). While mIgE does not induce degranulation or leukotriene synthesis, it leads to a more potent production of cytokines than IgE + Ag. Moreover, mIgE prevents the apoptosis of cytokine-deprived BMMCs, likely by maintaining Bcl-XL levels and producing autocrine-acting cytokines. The addition of Ag does not increase this IgE-induced survival. Since IgE concentrations as low as 0.1 μg/ml enhance BMMC survival, elevated plasma IgE levels in humans with atopic disorders may contribute to the elevated mast cell numbers seen in these individuals.
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