Negative feedback regulation of IgE synthesis by murine CD23

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作者：

P Yu，M Kosco-Vilbois，M Richards，G K?Hler，MC Lamers

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摘要：

IMMUNOGLOBULIN E is found in nanogram amounts in normal human and mouse serum. It is increased during parasitic infestations 1 and mediates allergy. CD23, the low-affinity receptor for IgE (FccRII), has been proposed as an important regulator of IgE synthesis 2–4 . The type-II transmembrane lectin 4 CD23 is expressed in the mouse on B cells and follicular dendritic cells. In humans there are two forms of CD23 which differ in their intracellular amino-terminal 6/7 amino acids 4 expression of the A-form corresponds to that of murine CD23, whereas the B-form is also found on T and other haematopoietic cells 4 . CD23 has been implicated in cellular adhesion 5 , antigen presentation 6 , as a growth and differentiation factor for human B, T and plasma cells and as a signal transduction molecule 7 (reviewed in refs 3, 8). Here we disrupt the gene coding for murine CD23 (ref. 9) to clarify the role of CD23 in vivo and find that B- and T-cell development is normal in these CD23-deficient mice. Immune responses to the helminth Nippostrongylus brasiliensis are unaffected. In contrast, immunization with thymus-dependent antigens leads to increased and sustained specific IgE antibody titres compared with controls. Formation of germinal centres is normal. These results suggest that murine CD23 acts as a negative feedback component of IgE regulation.

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关键词：

Negative feedback regulation of IgE synthesis by murine CD23, Artículo

DOI：

10.1038/369753a0

被引量：

665

年份：

1994