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

Michael Halpern, S. Schwartz

Research output: Contribution to journalArticle

11 Citations (Scopus)

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-γ (IFN-γ), and interferon-α (IFN-α) are involved in coordinate regulation of CD23. IL-4 stimulates production of both CD23 and IgE. IFN-γ also stimulates production of CD23, but suppresses production of IgE and inhibits IL-4-mediated production of CD23. IFN-α also suppresses these IL-4-mediated activities and, in addition, suppresses IFN-γ-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-γ. 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- γ and IL-4 may also be important in other allergic conditions, parasitic infections, and a variety of disease states.

Original languageEnglish (US)
Pages (from-to)197-200
Number of pages4
JournalInternational Archives of Allergy and Immunology
Volume100
Issue number3
StatePublished - 1993
Externally publishedYes

Fingerprint

IgE Receptors
Fc Receptors
Atopic Dermatitis
Interferons
Interleukin-4
Immunoglobulin E
Parasitic Diseases
Langerhans Cells
T-Lymphocytes
Skin

Keywords

  • CD23
  • Dermatitis
  • IgE
  • Immunoregulation
  • Interferon
  • Interleukin-4

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Regulation of the low affinity IgE Fc receptor (CD23) in atopic dermatitis. / Halpern, Michael; Schwartz, S.

In: International Archives of Allergy and Immunology, Vol. 100, No. 3, 1993, p. 197-200.

Research output: Contribution to journalArticle

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