Original article
Characterization of the mononuclear cell infiltrate in atopic dermatitis using monoclonal antibodies

https://doi.org/10.1016/0091-6749(83)90546-8Get rights and content

Abstract

Tissue sections from involved and uninvolved skin of nine patients with atopic dermatitis (AD) were investigated by light microscopy, electron microscopy, and an immunoperoxidase method using monoclonal antibodies to cell-surface antigens. Acute lesions were characterized by spongiotic epidermis, with increased numbers of infiltrating mononuclear cells consisting predominantly of lymphocytes. Perivascular dermal infiltrates consisted of lymphocytes and a few monocytes-macrophages. Capillary endothelial cells were not enlarged. In chronic lesions the epidermis was hyperplastic, with virtually no cellular infiltrate. The perivascular dermal infiltrates consisted primarily of monocytes-macrophages intermixed with lymphocytes. Capillary lumens were narrowed by enlarged endothelial cells. The majority of the infiltrating lymphocytes in all skin biopsy specimens from AD patients were stained with anti-T3, anti-Leu-1, anti-T4, and anti-Leu-3 antibodies, suggesting that most of the infiltrating lymphocytes were T cells possessing the helper/inducer phenotype. In contrast, a smaller number of infiltrating cells reacted with anti-T8 or anti-Leu-2 antibodies, which define the suppressor/cytotoxic T cell population. Langerhans cells, as defined by reactivity with anti-T6 monoclonal antibody, were increased in the diseased skin of AD patients. The presence of increased numbers of Langerhans cells and T cells of the helper I inducer phenotype may reflect increased antigen processing in the diseased skin of patients. In addition, the smaller number of T8+ cells infiltrating into the skin suggests that the depression of circulating T8 + cells observed in the majority of patients with AD is not due to the selective migration of these T8+ cells into the skin.

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    Supported by U.S.P.H.S. grants AM-16392, AI-05877, and CA-29061, HL-18646, and by grants from the Hood Foundation and the Rorer Co.

    R. S. G. is the recipient of Allergic Diseases Academic Award No. 1 KO7 AI 00440-01.

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