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CD23-mediated cell signalling
J P Kolb1, A Abadie, A Proschnicka-Chalufour
1U365 INSERM, Institut Curie, Paris, France.
Insights
This study reveals that CD23 (Fc epsilon RII) ligation triggers distinct signaling pathways in human B cells and monocytes. While B cells show calcium mobilization, both cell types exhibit cAMP accumulation, suggesting complex signal transduction.
Area of Science:
- Immunology
- Cell Biology
- Molecular Signaling
Background:
- CD23 (Fc epsilon RII) is a low-affinity receptor for IgE, playing a role in B cell regulation and immune responses.
- Understanding CD23-mediated signal transduction is crucial for deciphering its function in B cells and monocytes.
Purpose of the Study:
- To investigate the signal transduction pathways activated by CD23 ligation in human B cells and monocytes.
- To explore the potential cross-talk between CD23 and IL-4 signaling pathways.
Main Methods:
- Analysis of phosphoinositide hydrolysis and calcium mobilization in response to CD23 ligation using monoclonal antibodies and IgE+anti-IgE complexes.
- Measurement of cAMP accumulation following CD23 redistribution.
- Investigation of signaling cross-talk between CD23 and IL-4.
Main Results:
- CD23 ligation triggered phosphoinositide hydrolysis and calcium mobilization in B cells, but not in monocytes.
- Both B cells and monocytes showed cAMP accumulation upon CD23 redistribution.
- Evidence suggests cross-talk between IL-4 and CD23-induced second messengers.
Conclusions:
- CD23 ligation elicits differential signaling pathways in B cells and monocytes.
- The observed differences may be attributed to distinct CD23 isoforms and their associated molecules.
- CD23 signaling pathways exhibit cross-talk with IL-4-induced pathways, highlighting intricate cellular communication.
Abstract:
Signal transduction through ligation of the CD23 (Fc epsilon RII) molecule was analysed in human B cells and monocytes. Monoclonal antibodies directed against the IgE binding site of CD23 were found to trigger phosphoinositide hydrolysis and calcium mobilization in B cells, but not in monocytes. These early events were also obtained with an IgE+anti-IgE complex, which supposedly mimicks the physiological situation of a multivalent antigen inducing the cross-linking of cell-bound IgE. Redistribution of CD23 was also found to evoke cAMP accumulation both in B lymphocytes and monocytes. Moreover, we present evidence indicating a possible cross-talk between the IL-4- and CD23-induced second messengers. We suggest that the alternative transduction pathways elicited by ligation of CD23 are linked to the CD23 isoform(s) expressed by these cells and may result from their association with different sets of molecules.