Abstract
Immunoglobulin E (IgE) plays a central role in the pathogenesis of allergic diseases by interacting with two membrane receptors: high-affinity FcεRI and low-affinity FcεRII (CD23). Allergeninduced IgE-occupied FcεRI aggregation on the mast cell or basophil cell surface leads to the activation of intracellular signaling events and eventually the release of pre-formed and de novo synthesized inflammatory mediators. The role of FcεRII in allergic diseases has been proposed to include regulation of IgE synthesis, enhanced histamine release from basophils, and a contribution to Ag-IgE complex presentation but the exact function of CD23 remains poorly understood. This review summarizes some new developments in IgE Fc-receptor studies with an emphasis on regulation of FcεRI expression and signal transduction, including monomeric IgE, lipid raft segregation, and some recently identified negative regulators. A better understanding of signaling events following IgE FcR aggregation will shed new light on how allergy patients might be treated more safely and effectively.
| Original language | English |
|---|---|
| Pages (from-to) | 1-16 |
| Number of pages | 16 |
| Journal | Immunologic Research |
| Volume | 37 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2007 |
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All Science Journal Classification (ASJC) codes
- Immunology
Cite this
Decoding IgE Fc receptors. / Zhang, Ming; Murphy, Richard F.; Agrawal, Devendra K.
In: Immunologic Research, Vol. 37, No. 1, 01.2007, p. 1-16.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Decoding IgE Fc receptors
AU - Zhang, Ming
AU - Murphy, Richard F.
AU - Agrawal, Devendra K.
PY - 2007/1
Y1 - 2007/1
N2 - Immunoglobulin E (IgE) plays a central role in the pathogenesis of allergic diseases by interacting with two membrane receptors: high-affinity FcεRI and low-affinity FcεRII (CD23). Allergeninduced IgE-occupied FcεRI aggregation on the mast cell or basophil cell surface leads to the activation of intracellular signaling events and eventually the release of pre-formed and de novo synthesized inflammatory mediators. The role of FcεRII in allergic diseases has been proposed to include regulation of IgE synthesis, enhanced histamine release from basophils, and a contribution to Ag-IgE complex presentation but the exact function of CD23 remains poorly understood. This review summarizes some new developments in IgE Fc-receptor studies with an emphasis on regulation of FcεRI expression and signal transduction, including monomeric IgE, lipid raft segregation, and some recently identified negative regulators. A better understanding of signaling events following IgE FcR aggregation will shed new light on how allergy patients might be treated more safely and effectively.
AB - Immunoglobulin E (IgE) plays a central role in the pathogenesis of allergic diseases by interacting with two membrane receptors: high-affinity FcεRI and low-affinity FcεRII (CD23). Allergeninduced IgE-occupied FcεRI aggregation on the mast cell or basophil cell surface leads to the activation of intracellular signaling events and eventually the release of pre-formed and de novo synthesized inflammatory mediators. The role of FcεRII in allergic diseases has been proposed to include regulation of IgE synthesis, enhanced histamine release from basophils, and a contribution to Ag-IgE complex presentation but the exact function of CD23 remains poorly understood. This review summarizes some new developments in IgE Fc-receptor studies with an emphasis on regulation of FcεRI expression and signal transduction, including monomeric IgE, lipid raft segregation, and some recently identified negative regulators. A better understanding of signaling events following IgE FcR aggregation will shed new light on how allergy patients might be treated more safely and effectively.
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UR - http://www.scopus.com/inward/citedby.url?scp=34248367985&partnerID=8YFLogxK
U2 - 10.1007/BF02686092
DO - 10.1007/BF02686092
M3 - Review article
VL - 37
SP - 1
EP - 16
JO - Immunologic Research
JF - Immunologic Research
SN - 0257-277X
IS - 1
ER -