ISSN:
1365-2133
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Summary Intercellular adhesion molecule-1 (ICAM-1) expression is a necessary requirement for leucocyte/keratinocyte interactions, and keratinocyte upregulation of ICAM-1 is seen in several inflammatory dermatoses. While keratinocytes have a very low constitutive expression of ICAM-1, they can be induced to upregulate ICAM-1 in response to several inflammatory cytokines, such as interferon-γ (IFNγ). There is some evidence to suggest that the state of keratinocyte differentiation may influence the level of ICAM-1 expression induced by IFNγ. The purpose of this study was to investigate the hypothesis that keratinocytes, as they differentiate, may lose their ability to increase their expression of ICAM-1 in response to IFNγ. Keratinocytes from 13 donors were cultured under conditions which either permitted (Green's medium) or inhibited (MCDB153) differentiation. The ICAM-1 expression in response to IFNγ was assessed by a sensitive, cell-based. ELISA, and related to the state of differentiation of the cells (as assessed by a quantitative assay for involucrin). While keratinocytes grown in MCDB153 remained responsive to IFNγ throughout 4 days of culture, the response of keratinocytes grown in Green's medium progressively decreased, so that, by day 3, only a high concentration of IFNγ (500U/ml) led to a significant increase in ICAM-1 expression. After 4 days in culture, no upregulation of ICAM-1 was seen. The deterioration in the response of Green's-cultured keratinocytes to IFNγ mirrored an increase in their expression of involucrin in parallel cultures. Overall, our data demonstrate a progressive loss in the ability of keratinocytes to upregulate ICAM-1 in response to IFNγ, which is associated with differentiation of these cells. This would support the view that only basal proliferative keratinocytes are responsive to inflammatory cytokines, and play a part in the initiation and amplification of inflammatory reactions in vivo.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1365-2133.1996.d01-927.x
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