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Integrity of the permeability barrier regulates epidermal Langerhans cell density
Author(s) -
PROKSCH E.,
BRASCH J.,
STERRY W.
Publication year - 1996
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1996.66828.x
Subject(s) - transepidermal water loss , langerhans cell , barrier function , epidermis (zoology) , chemistry , immunoperoxidase , immunology , biology , microbiology and biotechnology , antigen , pathology , antibody , stratum corneum , medicine , anatomy , monoclonal antibody
Summary Previous studies have shown that barrier requirements regulate epidermal liquid and DNA synthesis. In the present study, we examined the possibility that the integrity of the permeability barrier influences epidermal Langerhans cells involved with the immune response. Barrier disruption was achieved by treatment of human skin with acetone, sodium dodecylsulphate (SDS), or tape stripping, until a 10–20‐fold increase in transepidermal water loss was achieved. Serial biopsies were performed 6–168 after treatment, and Langerhans cells were complexed with anti‐CD1a (Leu6) or S‐l00 antibodies, and visualized with an immunoperoxidase technique. Acetone treatment resulted in an increase in epidermal Langerhans cell density, reaching a maximum of 94% over control (P < 0.01) by 24 and 48 h post‐treatment. Following SDS treatment or tape stripping, epidermal Langerhans cell density was increased by 100 and 175% (P < 0.01), respectively. There was a linear correlation between the degree of barrier disruption and the increase in epidermal Langerhans cell density. Studies with the Ki‐S3 proliferation‐associated nuclear antigen revealed a two‐ to threefold increase in epidermal proliferation after barrier disruption. The time curves of the increase in Langerhans cell density and the increase in epidermal proliferation were similar, suggesting that there was a coordinate regulation. In contrast with our previous studies employing patch test reactions to allergens or irritants, disruption of barrier function neither resulted in an increased dermal Langerhans cell density, nor influenced T lymphocytes (CD3 + . Leu4 + ). Macrophages (KiM8 + ), ICAM‐1 or ELAM‐1 expression in the skin. In addition, barrier disruption did not result in either dermal inflammation or epidermal spongiosis. In summary these findings support our hypothesis that the permeability barrier influences epidermal Langerhans cell density, which is involved in maintaining an immunological barrier.