Negative feedback regulation of IgE synthesis by murine CD23

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Abstract
IMMUNOGLOBULIN E is found in nanogram amounts in normal human and mouse serum. It is increased during parasitic infestations1 and mediates allergy. CD23, the low-affinity receptor for IgE (FccRII), has been proposed as an important regulator of IgE synthesis2–4. The type-II transmembrane lectin4 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 acids4 expression of the A-form corresponds to that of murine CD23, whereas the B-form is also found on T and other haematopoietic cells4. CD23 has been implicated in cellular adhesion5, antigen presentation6, as a growth and differentiation factor for human B, T and plasma cells, and as a signal transduction molecule7 (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.