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Updated: Aug 11, 2026

Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
Published on: June 13, 2014
Biologically active intercellular adhesion molecule-1 is shed as dimers by a regulated mechanism in the inflamed
Mario Melis1, Elisabetta Pace, Liboria Siena
1Institute of Respiratory Physiopathology, Italian National Research Council, Palermo, Italy.
Insights
Soluble intercellular adhesion molecule-1 (sICAM-1) is released from cells in pleural effusions and can suppress immune responses by inhibiting cytotoxic lymphocyte adhesion.
Area of Science:
- Immunology
- Cell Biology
- Molecular Medicine
Background:
- Intercellular adhesion molecule-1 (ICAM-1) is vital for cell interactions in immune responses.
- Soluble ICAM-1 (sICAM-1) can modulate immunoinflammatory processes.
- Understanding sICAM-1 in disease is crucial for immune response modulation.
Purpose of the Study:
- Investigate the source, form, regulation, and function of sICAM-1 in pleural effusions.
- Determine the cellular origins and release mechanisms of sICAM-1.
- Assess the biological activity and immunosuppressive potential of sICAM-1.
Main Methods:
- Analysis of cells and pleural fluid from patients with cancer, tuberculosis, and heart failure.
- Characterization of sICAM-1 conformation and cellular expression.
- Investigation of sICAM-1 release mechanisms, including cytokine involvement.
- Functional assays to evaluate sICAM-1's effect on immune cell interactions.
Main Results:
- Dimeric sICAM-1 is locally released in tuberculous and malignant pleural effusions.
- sICAM-1 is shed from pre-existing surface ICAM-1, with leukocytes, epithelial, and mesothelial cells as sources.
- Pleural macrophages regulate sICAM-1 release via a tumor necrosis factor-alpha-dependent pathway.
- Pleural sICAM-1 inhibits conjugate formation between LAK cells and K562 cells.
Conclusions:
- sICAM-1 is shed in a regulated manner from multiple cell types within the pleural space.
- Pleural sICAM-1 exhibits immunosuppressive activity by hindering cytotoxic lymphocyte adhesion.
- sICAM-1 plays a significant role in modulating immune responses in pleural effusions.
Abstract:
Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that plays a crucial role in cell-cell interactions involved in the recruitment of cells and immune responses. Under some circumstances, ICAM-1 is found as a soluble protein that has the potential to influence the nature of immunoinflammatory responses. By examining cells and fluid from the pleural compartment of patients with cancer, tuberculosis, and congestive heart failure, the cellular source, conformation, control, and biological activity of soluble ICAM-1 (sICAM-1) were investigated. The results suggest that dimeric sICAM-1 was released locally in the pleural compartment of tuberculous and malignant effusions. sICAM-1 was shed from preexpressed surface ICAM-1 rather than produced de novo, and both CD45-positive leukocytes and cytokeratin-positive epithelial and mesothelial cells expressed ICAM-1, suggesting multiple cellular sources for sICAM-1. The expression of sICAM-1 was regulated because pleural macrophages caused release of sICAM-1 via a tumor necrosis factor-alpha-dependent mechanism. The functional significance of sICAM-1 was demonstrated by showing that pleural sICAM-1 interfered with conjugate formation between LAK cells and K562 cells, suggesting that pleural sICAM-1 plays an immunosuppressive role by inhibiting adhesion of cytotoxic lymphocytes and tumor cells. Thus, sICAM-1 is shed from the surface of cells in a regulated manner and has the potential to influence the immune response in the pleural space.
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