• Journal Article

Regulation of the low affinity IgE Fc receptor (CD23) in atopic dermatitis

Citation

Halpern, M., & Schwartz, S. (1993). Regulation of the low affinity IgE Fc receptor (CD23) in atopic dermatitis. International Archives of Allergy and Immunology, 100(3), 197-200.

Abstract

Alterations in the production of CD23, the IgE Fc receptor, may play a role in the etiology of atopic dermatitis and other allergic conditions. Interleukin-4 (IL-4), interferon-gamma (IFN-gamma), and interferon-alpha (IFN-alpha) are involved in coordinate regulation of CD23. IL-4 stimulates production of both CD23 and IgE. IFN-gamma also stimulates production of CD23, but suppresses production of IgE and inhibits IL-4-mediated production of CD23. IFN-alpha also suppresses these IL-4-mediated activities and, in addition, suppresses IFN-gamma-mediated stimulation of CD23 production. Changes in this coordinate regulation may be involved in the development of atopic dermatitis. Expression of CD23 by Langerhans cells is stimulated by IL-4 and IFN-gamma. Further, levels of CD23-positive T cells are elevated in atopic dermatitis subjects as compared to non-atopic controls, and observed skin changes appear to be related to changes in CD23-positive mononuclear cell populations. Coordinate regulation of CD23 by IFN-gamma and IL-4 may also be important in other allergic conditions, parasitic infections, and a variety of disease states.