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Updated: Apr 5, 2026

Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro
Published on: November 26, 2018
CD100 and plexins B2 and B1 mediate monocyte-endothelial cell adhesion and might take part in atherogenesis
Maria Carolina A Luque1, Paulo S Gutierrez2, Victor Debbas2
1Heart Institute of São Paulo (InCor), HC-FMUSP, São Paulo, SP, Brazil; Clinical Immunology and Allergy, Department of Clinical Medicine, University of São Paulo Medical School-HC-FMUSP, São Paulo, SP, Brazil.
Insights
CD100 and plexins are key adhesion molecules in monocyte-endothelial cell binding, crucial for immune cell function and potentially atherosclerosis. Targeting these molecules may offer new therapeutic strategies.
Area of Science:
- Immunology
- Cell Biology
- Cardiovascular Research
Background:
- Leukocyte migration is vital for immune responses, involving interactions between leukocytes and endothelial cells (ECs).
- Previous research identified adhesion molecules in this process, but CD100 and plexins' roles remain under investigation.
- CD100 is implicated in platelet-endothelial cell interactions relevant to atherosclerosis.
Purpose of the Study:
- To investigate the role of CD100 and plexins in monocyte-endothelial cell (EC) binding.
- To identify potential receptors for CD100 on monocytes.
- To explore CD100 and plexins as therapeutic targets in monocyte adhesion and atherosclerosis.
Main Methods:
- Detected CD100 expression in monocytes, macrophages, foam cells, and endothelial cells.
- Identified plexin B2 as a potential CD100 receptor on monocytes.
- Utilized blocking experiments with antibodies against CD100, plexin B1, and plexin B2 in monocyte-EC adhesion assays.
Main Results:
- CD100 is expressed on both monocytes and endothelial cells.
- Plexin B2 was identified as a putative CD100 receptor on monocytes.
- Blocking CD100, plexin B1, or plexin B2 significantly inhibited monocyte-EC adhesion.
- CD100 and plexins function as adhesion molecules in monocyte-EC binding, potentially mediated by endothelial plexin B1 and monocytic plexin B2.
Conclusions:
- CD100 and plexins play a significant role in monocyte-endothelial cell adhesion.
- These molecules may be involved in the pathogenesis of atherosclerosis.
- CD100 and plexins represent potential therapeutic targets for conditions involving monocyte adhesion.
Abstract:
Leukocyte migration is essential for the function of the immune system. Their recruitment from the vessels to the tissues involves sequential molecular interactions between leukocytes and endothelial cells (ECs). Many adhesion molecules involved in this process have already been described. However, additional molecules may be important in this interaction, and here we explore the potential role for CD100 and plexins in monocyte-EC binding. CD100 was shown to be involved in platelet-endothelial cell interaction, an important step in atherogenesis and thrombus formation. In a recent work we have described CD100 expression in monocytes and in macrophages and foam cells of human atherosclerotic plaques. In the present work, we have identified plexin B2 as a putative CD100 receptor in these cells. We have detected CD100 expression in the endothelium as well as in in vitro cultured endothelial cells. Blocking of CD100, plexin B1 and/or B2 in adhesion experiments have shown that both CD100 and plexins act as adhesion molecules involved in monocyte-endothelial cell binding. This effect may be mediated by CD100 expressed in both cell types, probably coupled to the receptors endothelial plexin B1 and monocytic plexin B2. These results can bring new insights about a possible biological activity of CD100 in monocyte adhesion and atherosclerosis, as well as a future candidate for targeting therapeutics.
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