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Langerhans' cells and lymphocytic infiltrate in AIDS-associated Kaposi's sarcoma. An immunohistochemical study
F Valcuende-Cavero1, M I Febrer-Bosch, A Castells-Rodellas
1Dermatology Unit, Hospital Gran Vía, Castellón, Spain.
Insights
Skin immune cells, Langerhans
Area of Science:
- Immunology
- Dermatology
- Oncology
Background:
- Epidermal Langerhans' cells are key to skin immunity.
- Human immunodeficiency virus (HIV) uses CD4 receptors.
- Kaposi's sarcoma (KS) primarily affects the skin.
Purpose of the Study:
- To investigate the role of skin immune cells in AIDS-associated Kaposi's sarcoma.
- To evaluate the density and phenotype of dendritic epidermal cells and inflammatory infiltrates in KS lesions.
Main Methods:
- Studied 12 patients with AIDS-associated KS.
- Used monoclonal antibodies and avidin-biotin-peroxidase technique on frozen skin sections.
- Evaluated antigens CD1a, HLA-DR, CD4, CD3, and CD8.
Main Results:
- Reduced number of Langerhans' cells in AIDS-KS skin lesions.
- Significant decrease in HLA-DR expressing cells and CD4+ cells.
- Tumor infiltrate composed mainly of CD3+ CD8+ lymphocytes.
- Dermal CD4+ dendritic cells and focal HLA-DR on keratinocytes observed.
Conclusions:
- Altered Langerhans' cell phenotype and local immune imbalance may promote KS lesion growth.
- Findings highlight the role of skin immunity in AIDS-associated Kaposi's sarcoma pathogenesis.
Abstract:
The epidermal Langerhans' cells are dendritic cells of the skin capable of triggering cutaneous immune responses. They possess the membrane antigens required to this effect: class II histocompatibility antigen, CD1a and CD4; the latter acts as receptor for the human immunodeficiency virus. The skin is the organ primarily affected by Kaposi's sarcoma (KS). In epidemic KS, the local immunologic conditions of the skin are little known. We therefore studied 12 patients with AIDS-associated KS, evaluating the density and phenotypic expression in KS-affected and unaffected skin of the following antigens: CD1a, HLA-DR, CD4 in dendritic epidermal cells and dermis, and CD3, CD4 and CD8 in cells of the inflammatory infiltrate, using monoclonal antibodies applied to frozen sections with the avidin-biotin-peroxidase technique. Langerhans' cells in the AIDS-KS skin lesions were found to be decreased in number. This decrease was even more pronounced in the case of cells expressing HLA-DR antigen. A number of them were also revealed with CD4. The tumour lymphocytic infiltrate was almost exclusively composed of CD3+ CD8+ phenotype lymphocytes. The dermis also revealed CD4+ dendritic cells. The basal keratinocytes focally expressed HLA-DR. These phenotypical alterations of the Langerhans' cells and the local immunological imbalance observed may contribute to the growth and continuity of the KS lesions.