Preferential Signaling and Induction of Allergy-promoting Lymphokines Upon Weak Stimulation of the High Affinity IgE Receptor on Mast Cells

التفاصيل البيبلوغرافية
العنوان:	Preferential Signaling and Induction of Allergy-promoting Lymphokines Upon Weak Stimulation of the High Affinity IgE Receptor on Mast Cells
المؤلفون:	Gonzalez-Espinosa, Claudia, Odom, Sandra, Olivera, Ana, Hobson, J. Peyton, Martinez, Maria Eugenia Cid, Oliveira-dos-Santos, Antonio, Barra, Lillian, Spiegel, Sarah, Penninger, Josef M., Rivera, Juan
المصدر:	The Journal of Experimental Medicine; June 2003, Vol. 197 Issue: 11 p1453-1465, 13p
مستخلص:	Mast cell degranulation and de novo cytokine production is a consequence of antigen-aggregation of the immunoglobulin E (IgE)-occupied high affinity receptor for IgE (FcεRI). Herein, we report that lymphokines that promote allergic inflammation, like MCP-1, were potently induced at low antigen (Ag) concentrations or at low receptor occupancy with IgE whereas some that down-regulate this response, like interleukin (IL)-10, required high receptor occupancy. Weak stimulation of mast cells caused minimal degranulation whereas a half-maximal secretory response was observed for chemokines and, with the exception of TNF-α, a weaker cytokine secretory response was observed. The medium from weakly stimulated mast cells elicited a monocyte/macrophage chemotactic response similar to that observed at high receptor occupancy. Weak stimulation also favored the phosphorylation of Gab2 and p38MAPK, while LAT and ERK2 phosphorylation was induced by a stronger stimulus. Gab2-deficient mast cells were severely impaired in chemokine mRNA induction whereas LAT-deficient mast cells showed a more pronounced defect in cytokines. These findings demonstrate that perturbation of small numbers of IgE receptors on mast cells favors certain signals that contribute to a lymphokine response that can mediate allergic inflammation.
قاعدة البيانات:	Supplemental Index

الوصف
تدمد:	00221007 15409538
DOI:	10.1084/jem.20021806