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Mouse CD23 regulates monocyte activation through an interaction with the adhesion molecule CD11b/CD18
S Lecoanet-Henchoz1, C Plater-Zyberk, P Graber
1Geneva Biomedical Research Institute, Glaxo Wellcome Research and Development, Switzerland.
European Journal of Immunology
|October 28, 1997
Summary
Murine CD23 interacts with the CD11b adhesion molecule on myeloid cells, impacting interleukin-6 production. Blocking this interaction may offer therapeutic benefits for inflammatory conditions like arthritis.
Area of Science:
- Immunology
- Cell Biology
- Molecular Medicine
Background:
- CD23 is expressed on hemopoietic cells and plays a role in immune responses.
- Previous studies showed blocking CD23 improves arthritis severity in a murine model.
Purpose of the Study:
- To investigate the interaction between murine CD23 and CD11b on myeloid cells.
- To understand the functional consequences of this interaction on cytokine production and identify regulatory loops.
Main Methods:
- Utilized a recombinant fusion protein (ZZ-CD23) to study CD23 binding.
- Employed anti-CD11b monoclonal antibodies to inhibit interactions.
- Measured interleukin-6 (IL-6) production and assessed autocrine regulation.
Main Results:
- Murine CD23 binds to CD11b on macrophages and monocytes.
- Anti-CD11b antibodies significantly inhibit ZZ-CD23 binding.
- ZZ-CD23 binding up-regulates IL-6 production, which in turn enhances CD23 binding to macrophages.
Conclusions:
- Murine CD23 interacts with CD11b, a surface adhesion molecule on myeloid cells.
- This interaction regulates myeloid cell biological activities, including IL-6 production.
- A positive autocrine loop involving IL-6 and CD23 binding suggests a novel regulatory mechanism in myeloid cells.