Cellular requirements of IgE-antibody regulation.
The low affinity receptor for IgE ( Fc epsilon RII), which is identical to CD 23 has been recently implicated in a variety of functions. It appears as an early stage specific marker in the ontogeny of the IgM-bearing B cell. In humans the CD 23 is also exposed on T-cells in patients with elevated IgE, while in rodents Fc epsilon RII seems to be mainly present on T-lymphocytes. Fc epsilon RII can also be detected on macrophages, eosinophils and platelets. Activation of these cells induces an amplification of the inflammatory response. It is currently suggested that IgE-binding molecules, which are related to CD 23, modulate IgE synthesis according to their degree of glycosylation. Evidence has been provided recently that interleukin 4 induces the expression of Fc epsilon RII (CD23). The action of interleukins, IgE binding factors and cytokines on the complex events of IgE-induction and synthesis are currently studied.[1]References
- Cellular requirements of IgE-antibody regulation. König, W., Pfeil, P., Hofmann, U., Bujanowski-Weber, J., Knöller, I. Allergologia et immunopathologia. (1988) [Pubmed]
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