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American Journal of Pathology, Vol 140, 1365-1374, Copyright © 1992 by American Society for Investigative Pathology

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HUT 78 T cells bind to noncytokine-stimulated keratinocytes using a non- CD18-dependent adhesion pathway

BJ Nickoloff, RS Mitra, Y Shimizu, JN Barker, G Karabin, T Stoof and LM Stoolman
Department of Pathology, University of Michigan Medical Center, Ann Arbor.

The initial in vitro observation that cultured keratinocytes, when treated with cytokines such as gamma interferon, increased the binding of T lymphocytes, opened up a whole new avenue of research to understand epidermal trafficking patterns in inflammatory skin diseases. A growing body of data strongly supports the in vivo role of lymphocyte-function-associated antigen-1 (CD18) expression by T cells in the binding to intercellular adhesion molecule-1 (CD54) expressing keratinocytes. To further explore the molecular basis for other possible adhesive interactions involving T cells and skin-derived cellular constituents, the authors used 2 cell lines (HUT 78 cells and Jurkat cells) and added them to multipassaged human keratinocytes, fibroblasts, and melanocytes. The skin-derived cells were treated with cytokines alone, or in combination, with a phorbol ester. HUT cells were capable of binding to keratinocytes in the absence of pretreatment with cytokines at 25 degrees C, which was not inhibited by anti-CD18 antibodies, or sensitive to reducing the temperature of the adhesion assay to 7 degrees C. Fibroblasts and melanocytes also constitutively bound HUT cells, but the binding to fibroblasts was highly temperature- sensitive. When keratinocytes were pretreated for 48 hours with gamma interferon plus phorbol ester, a "superadhesive" state was induced, resulting in a synergistically increased binding ability of both HUT cells and Jurkat cells. This effect was related to quantitative increases in keratinocyte intercellular adhesion molecule-1 expression. Several other clear-cut qualitative and quantitative differences were detectable in the ability of HUT cells and JS cells to bind to nontreated and cytokine/phorbol ester-treated keratinocytes, fibroblasts, and melanocytes. These results emphasize the complexity of molecular associations underlying T-cell trafficking patterns, potentially operative in the dermal and epidermal compartments of the skin.

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