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Published on: October 20, 2014
[Physiopathological role of low affinity IgE receptor (CD23) in hematopoietic cells]
J P Kolb1, N Paul-Eugène, F Ouaaz
1Unité INSERM U365, Institut Curie, Paris.
Insights
Signaling through the low-affinity IgE receptor (CD23) varies by cell type. Monocytes utilize a pathway involving nitric oxide synthase, which is amplified in allergic diseases, impacting immune cell function.
Area of Science:
- Immunology
- Cell Signaling
Context:
- The low-affinity IgE receptor (CD23) plays a role in immune responses.
- CD23 signaling pathways differ across cell types, influencing cellular functions.
Purpose:
- To investigate the distinct signaling pathways triggered by CD23 ligation in B lymphocytes and monocytes.
- To elucidate the role of CD23 signaling in monocyte differentiation and inflammatory responses.
Summary:
- CD23 ligation in B cells activates phospholipase C and cAMP accumulation via a Pertussis toxin-insensitive G-protein.
- In monocytes (CD23b isoform), CD23 ligation induces delayed cAMP accumulation dependent on cGMP and nitric oxide synthase activation.
- This monocyte CD23 pathway is exacerbated in allergic diseases and affects cell differentiation, mediator release, and cytotoxicity.
Impact:
- Understanding CD23 signaling in monocytes provides insights into allergic disease pathogenesis.
- Identifies a novel pathway influencing monocytic lineage differentiation and inflammatory mediator release.
- Highlights the potential of targeting CD23-mediated monocyte signaling in treating allergic conditions.
Abstract:
Ligation of the low affinity IgE receptor by specific monoclonal antibodies or multivalent IgE complexes result in the transduction of signals which differ according to the CD23 isotype expressed by the various cell types. In B lymphocytes, it elicits the early activation of phospholipase C through a mechanism involving a G-protein insensitive to Pertussis toxin, followed by a late phase of cAMP accumulation. In monocytes, which express the CD23b isoform, ligation of CD23 was also found to induce a delayed accumulation of cAMP, that was largely dependent on a prior cGMP increase through a mechanism involving the activation of a NO synthase. This pathway, which appears to be exacerbated in allergic diseases, seems to play an important role in the differentiation of cells of the monocytic lineage, their capacity to release proinflammatory mediators and their cytotoxic functions.
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