Presented in part at the Central Region Society for Investigative Dermatology 11 November 1988; at the 47th Annual Meeting of the American Academy of Dermatology, 5 December 1988; and the Tricontinental Meeting of the Society for Investigative Dermatology, 29 April 1989.
Differential modulation of keratinocyte intercellular adhesion molecule-i expression by gamma interferon and phorbol ester: evidence for involvement of protein kinase C signal transduction
Article first published online: 29 JUL 2006
British Journal of Dermatology
Volume 122, Issue 3, pages 333–342, March 1990
How to Cite
GRIFFITHS, C.E.M., ESMANN, J., FISHER, G.J., VOORHEES, J.J. and NICKOLOFF, B.J. (1990), Differential modulation of keratinocyte intercellular adhesion molecule-i expression by gamma interferon and phorbol ester: evidence for involvement of protein kinase C signal transduction. British Journal of Dermatology, 122: 333–342. doi: 10.1111/j.1365-2133.1990.tb08281.x
- Issue published online: 29 JUL 2006
- Article first published online: 29 JUL 2006
- Accepted for publication 20 September 1989
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.