Ligation of CD23 triggers cAMP generation and release of inflammatory mediators in human monocytes

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N Paul-Eugene1, J P Kolb, A Abadie

  • 1Département d'Immunologie, Institut Henri Beaufour, Les Ulis, France.

Journal of Immunology (Baltimore, Md. : 1950)
|November 1, 1992
PubMed

Insights

CD23 ligation on human monocytes triggers cyclic AMP (cAMP) generation, not calcium mobilization. This CD23-mediated cAMP increase influences monocyte activation, including IL-6 and thromboxane B2 production, regulating IgE-dependent functions.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • CD23, also known as Fc epsilon RII, is a low-affinity IgE receptor expressed on various immune cells.
  • Its precise role in monocyte signaling and activation remains incompletely understood.

Purpose of the Study:

  • To investigate the signaling pathways activated by CD23 ligation in normal human monocytes.
  • To determine if CD23 engagement can induce calcium mobilization or modulate intracellular cAMP levels.

Main Methods:

  • Human monocytes were stimulated with IL-4 to upregulate CD23 expression.
  • Monocytes were treated with anti-CD23 monoclonal antibodies (mAbs) and IgE/anti-IgE immune complexes.
  • Intracellular calcium mobilization ([Ca2+]i) and cyclic adenosine monophosphate (cAMP) levels were measured.
  • Production of IL-6 and thromboxane B2 was assessed.

Main Results:

  • CD23 ligation did not induce calcium mobilization in monocytes, unlike in B lymphocytes.
  • CD23 engagement led to a dose-dependent increase in intracellular cAMP in monocytes.
  • Anti-CD23 mAbs and IgE/anti-IgE complexes induced IL-6 and thromboxane B2 generation by CD23+ monocytes.
  • cAMP generation was confirmed to be CD23-mediated and not significantly affected by indomethacin.

Conclusions:

  • CD23 ligation on human monocytes induces cAMP generation, not calcium flux.
  • CD23 plays a role in regulating monocyte activation and IgE-dependent functions.
  • These findings highlight a novel signaling pathway for CD23 in monocytes.

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