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Vascular adhesion molecules in oral lichen planus
J A Regezi1, N P Dekker, L A MacPhail
1Department of Stomatology, School of Dentistry, University of California, San Francisco, USA.
Summary
Upregulation of adhesion molecules like ELAM-1, ICAM-1, and VCAM-1 in lichen planus may drive disease pathogenesis. Leukocyte receptors L-selectin, LFA-1, and VLA4 are expressed on infiltrating cells, aiding recruitment and retention in active lesions.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Lymphoid cell recruitment and retention are crucial in lichen planus pathogenesis.
- Adhesion molecules play a significant role in immune cell trafficking.
Purpose of the Study:
- To compare the expression and distribution of vascular adhesion molecules and leukocyte adhesion molecule ligands in lichen planus biopsies.
- To elucidate the role of these molecules in the disease's pathogenesis.
Main Methods:
- Immunohistochemical analysis of frozen sections from 12 lichen planus cases and 9 controls.
- Evaluation of vascular adhesion molecules (ELAM-1, P-selectin, ICAM-1, VCAM-1, PECAM-1, CD34) and leukocyte adhesion molecule ligands (LFA-1, Mac-1, VLA4, L-selectin).
- Semiquantitative assessment of staining intensity in three microvascular compartments.
Main Results:
- Lichen planus showed increased staining for ELAM-1, P-selectin, ICAM-1, and VCAM-1 in microvascular compartments, particularly VCAM-1 in the subepithelial plexus.
- Lichen planus infiltrates exhibited high expression of ICAM-1, L-selectin, LFA-1, and VLA4 on infiltrating cells.
- Normal controls displayed distinct staining patterns, with intense PECAM and weak VCAM-1 expression.
Conclusions:
- Upregulation of ELAM-1, ICAM-1, and VCAM-1 on endothelial cells likely contributes to lichen planus pathogenesis.
- Expression of leukocyte receptors L-selectin, LFA-1, and VLA4 on infiltrating cells suggests their role in immune cell recruitment and retention in active lesions.