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THE BIOLOGY OF IGE AND THE BASIS OF ALLERGIC DISEASE
Allergic individuals exposed to minute quantities of allergen experience an immediate response. Immediate hypersensitivity reflects the permanent sensitization of mucosal mast cells by allergen-specific IgE antibodies bound to their high-affinity receptors (Fc RI). A combination of factors contribut...
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Published in: | Annual review of immunology 2003-01, Vol.21 (1), p.579-628 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Allergic individuals exposed to minute quantities of allergen experience an
immediate response. Immediate hypersensitivity reflects the permanent
sensitization of mucosal mast cells by allergen-specific IgE antibodies bound
to their high-affinity receptors (Fc RI). A combination of factors
contributes to such long-lasting sensitization of the mast cells. They include
the homing of mast cells to mucosal tissues, the local synthesis of IgE, the
induction of Fc RI expression on mast cells by IgE, the consequent
downregulation of FcγR (through an insufficiency of the common
γ-chains), and the exceptionally slow dissociation of IgE from
Fc RI. To understand the mechanism of the immediate hypersensitivity
phenomenon, we need explanations of why IgE antibodies are synthesized in
preference to IgG in mucosal tissues and why the IgE is so tenaciously retained
on mast cell-surface receptors. There is now compelling evidence that the
microenvironment of mucosal tissues of allergic disease favors class switching
to IgE; and the exceptionally high affinity of IgE for Fc RI can now be
interpreted in terms of the recently determined crystal structures of
IgE-Fc RI and IgG-FcγR complexes. The rate of local IgE synthesis
can easily compensate for the rate of the antibody dissociation from its
receptors on mucosal mast cells. Effective mechanisms ensure that allergic
reactions are confined to mucosal tissues, thereby minimizing the risk of
systemic anaphylaxis. |
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ISSN: | 0732-0582 1545-3278 |
DOI: | 10.1146/annurev.immunol.21.120601.141103 |