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Published on: October 18, 2016
CD11c/CD18 Dominates Adhesion of Human Monocytes, Macrophages and Dendritic Cells over CD11b/CD18
Noémi Sándor1, Szilvia Lukácsi2, Rita Ungai-Salánki3
1MTA-ELTE Immunology Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
Insights
Complement receptors CD11b/CD18 (CR3) and CD11c/CD18 (CR4) mediate cell adhesion. CD11c dominates fibrinogen binding, with CD11b competition influencing myeloid cell attachment.
Area of Science:
- Immunology
- Cell Biology
- Biophysics
Background:
- Complement receptors CR3 (CD11b/CD18) and CR4 (CD11c/CD18) are beta2 integrins expressed on human myeloid cells.
- Previous research indicated CR3's primary role in phagocytosis over CR4.
- Fibrinogen is a common ligand for both CR3 and CR4.
Purpose of the Study:
- To investigate the distinct roles of CD11b and CD11c in cell adhesion to fibrinogen.
- To quantify CD11b and CD11c expression levels on human monocytes, macrophages (MDMs), and dendritic cells (MDDCs).
- To elucidate the functional interplay between CD11b and CD11c in mediating cell-fibrinogen interactions.
Main Methods:
- Bead-based technique for quantifying CD11b and CD11c surface expression.
- State-of-the-art biophysical techniques to measure cellular adhesion strength.
- Blocking studies using antibodies against CD11b to assess its inhibitory effect on adhesion.
Main Results:
- CD11c expression is preponderant in MDDCs, while CD11b is more dominant in monocytes.
- Cellular adhesion to fibrinogen is primarily mediated by CD11c.
- Blocking CD11b significantly enhanced MDDC and MDM attachment to fibrinogen, revealing competitive binding.
Conclusions:
- CD11c plays a dominant role in the adhesion of myeloid cells to fibrinogen.
- A competitive interaction exists between CD11b and CD11c for fibrinogen binding.
- A model was developed explaining differential cell adhesion behavior based on receptor numbers and binding strength.
Abstract:
Complement receptors CR3 (CD11b/CD18) and CR4 (CD11c/CD18) belong to the family of beta2 integrins and are expressed mainly by myeloid cell types in humans. Previously, we proved that CR3 rather than CR4 plays a key role in phagocytosis. Here we analysed how CD11b and CD11c participate in cell adhesion to fibrinogen, a common ligand of CR3 and CR4, employing human monocytes, monocyte-derived macrophages (MDMs) and monocyte-derived dendritic cells (MDDCs) highly expressing CD11b as well as CD11c. We determined the exact numbers of CD11b and CD11c on these cell types by a bead-based technique, and found that the ratio of CD11b/CD11c is 1.2 for MDDCs, 1.7 for MDMs and 7.1 for monocytes, suggesting that the function of CD11c is preponderant in MDDCs and less pronounced in monocytes. Applying state-of-the-art biophysical techniques, we proved that cellular adherence to fibrinogen is dominated by CD11c. Furthermore, we found that blocking CD11b significantly enhances the attachment of MDDCs and MDMs to fibrinogen, demonstrating a competition between CD11b and CD11c for this ligand. On the basis of the cell surface receptor numbers and the measured adhesion strength we set up a model, which explains the different behavior of the three cell types.
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