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Human Fc ε RII/CD23 in the Regulation of the Allergic Immune Response

Authors: E. P. Rieber; U. Pirron; N. Endres; J. C. Prinz;

Human Fc ε RII/CD23 in the Regulation of the Allergic Immune Response

Abstract

The human low affinity receptor for IgE (Fc e RII), also known as the leukocyte differentiation antigen CD23 [1], is a type II integral membrane glycoprotein of 45 kDa which is constitutively expressed on resting, β + /δ + B lymphocytes and is lost after isotype switch. Fc e RII/CD23 is also found on follicular dendritic cells, eosinophils, platelets, alveolar macrophages and can be induced on monocytes and Langerhans cells by IL-4. Two isoforms (CD23a and CD23b) differing in the N-terminal cytoplasmic part have been identified by molecular cloning. Soluble IgE binding fragments (sCD23) are released from CD23+ cells by proteolytic cleavage. Pleiotropic activities have been proposed for the Fc e RII/CD23 and its soluble derivatives. Although specific functions in IgE regulation have been described, the biological role of the CD23 molecule remains elusive. Two recently recognized characteristics of the Fc e RII/CD23 will be presented: 1) specific induction of CD23 on T-cells by allergens and 2) focusing of antigen via CD23.

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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Average
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