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. 1982 Jul;2(3 Suppl):111S-119S.

Use of monoclonal antibodies specific for T cell subsets in cutaneous disorders: II. Immunomorphological studies in blood and skin lesions

  • PMID: 6982276

Use of monoclonal antibodies specific for T cell subsets in cutaneous disorders: II. Immunomorphological studies in blood and skin lesions

D Schmitt et al. J Clin Immunol. 1982 Jul.

Abstract

The phenotype of the cutaneous immunocompetent cells in lesions of cutaneous T cell lymphoma (mycosis fungoides, Sézary syndrome), lichen planus, and chronic graft-vs.-host reaction infiltrates, was examined by the use of monoclonal antibodies directed against T cell populations and Langerhans cells (OKT3, OKT4, OKT5, OKT6, OKT8) (BL2, BL6). In Sézary syndrome, the phenotype of the Sézary cell is homogeneous (OKT3+, OKT4+, OKT8-, OKT6-, BL2-) and corresponds to the phenotype expressed by the normal helper T cell population. At the ultrastructural level, the discontinuous distribution of OKT4 and OKT3 antigenic sites on the cell surface is similar to the HTLA antigens. In skin lesions, the Langerhans cells expressed two specificities shared by normal thymocytes (OKT6 and BL6). We propose that the expression of these antigens could be related to the epithelial microenvironment (epithelium-dependent differentiation antigens). The tumoral lymphoid cells infiltrating the skin showed the same phenotype (helper type) as the circulating Sézary cells (OKT3+, OKT4+, OKT8-, OKT6-). Moreover, the OKT3+ cells also expressed HLA-DR antigens and corresponded to activated T lymphocytes. In lichen planus, our results suggest an immunological reaction similar to a delayed hypersensitivity reaction which includes all of the immunocompetent cell subpopulations, with a first stage of formation by Langerhans cells (OKT6+, BL6+, HLA-DR+) and helper cells, and a second stage mediated by suppressor/cytotoxic cells. The results from the study of graft-vs.-host reaction also suggest a cytotoxic effect mediated by suppressor/cytotoxic cells (OKT3+, OKT4-, OKT8+, HLA-DR+).

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