Differential modulation of keratinocyte intercellular adhesion molecule-i expression by gamma interferon and phorbol ester: evidence for involvement of protein kinase C signal transduction

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Abstract
There is growing evidence that keratinocytc (KC) intercellular adhesion molecule‐i (ICAM‐i) expression is involved in the epidermal trafficking øf T lymphocytes. To further characterize the molecular basis of KC ICAM‐i expression, the detailed kinetics of induction by gamma interferon (IFN‐γ)) as well as the phorbol ester, 12‐O tetradecanoylphorbol‐13‐acetate (TPA), were studied. This study reports that KCs express both the class II major histocompatibility antigen (HLA‐DR) and ICAM‐i in response to IFN‐γ, although the response is distinctive for each molecule. Also, TPA induces ICAM‐i, but not HLA‐DR expression, whilst the protein kinase inhibitor, H7, blocks the TPA, but not the IFN‐γ‐mediated response. The results provide a molecular basis whereby non‐cytokine‐mediated stimuli (e.g. TPA) alter KC signal transduction events involving protein kinase‐C (PK‐C) and thereby generate such immunologically relevant events as ICAM‐i expression. Thus, KCs may be targets for both T‐cell derived cytokines (e.g. IFN‐γ), and non‐cytokine TPA‐like molecules which stimulate PK‐C. Induction of ICAM‐i by either mechanism would be capable of instigating intraepidermal T‐cell trafficking.

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