Korean J Dermatol.
2000 Oct;38(10):1294-1302.
Expression of Cutaneous Lymphocyte-Associated Antigen in Psoriasis
- Affiliations
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- 1Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
Abstract
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BACKGROUND: The evidence that T lymphocytes play a key role in the pathogenesis of psoriasis is compelling. Memory T cells that infiltrate the skin express a unique skin-homing receptor called cutaneous lymphocyte-associated antigen (CLA). CLA is thought to target skin-associated T cells to inflammatory skin sites by interacting with endothelial cell ligand E-selectin. OBJECTIVE: The purpose of this study was to investigate the expression and pathogenetic roles of CLA in psoriasis. METHODS: We performed an immunohistochemical staining on the lesional and nonlesional skin specimens of 13 cases of chronic plaque type psoriasis and 5 skin specimens of normal persons as control group using seven monoclonal antibodies for CLA, CD3, CD4, CD8, CD20, CD45RO, and HLA- DR. Standard streptavidin-biotin peroxidase method using the monoclonal antibodies with AEC was used. RESULTS: CLA was expressed over 75% of mononuclear cells in the psoriatic epidermis and about 50% in the psoriatic dermis. CD3 was expressed in 50-90% of mononuclear cells in psoriatic epidermis and dermis. CD4 was expressed less than 10% in the psoriatic epidermis and 10-50% in the psoriatic dermis. In contrast, CD8 showed the strong reactivity in psoriatic epidermis (50-75%) and dermis (25-75%). CD20, the marker of B cell, was not expressed in the psoriatic epidermis and expressed in less than 25% in the psoriatic dermis. CD45RO, expressed on the memory T cells, was observed in less than 10% in the psoriatic epidermis but more than 75% in the psoriatic dermis. HLA-DR, the marker of activated lymphocytes, was expressed in less than 10% in the psoriatic epidermis and 25-50% in the psoriatic dermis. CONCLUSION: These results suggest that CLA may play a key role in the pathogenesis of psoriasis. In susceptible individuals, inciting factors, such as infection with streptococci, may activate the expression of CLA on T lymphocytes. CLA+ CD4+ T lymphocytes may be extravasated via CLA/E-selecin interaction and activated T lymphocytes could get together in the papillary dermis. Activated skin-homing CD4+ T lymphocytes arouse dormant intraepidermal CD8+ T lymphocytes. These CD8+ T lymphocytes may proliferate and produce cytokines and growth factors that trigger the chain reaction of cellular and molecular events to produce psoriatic plaques.