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*
Institute of Immunology, University Hospital Benjamin Franklin, Free University Berlin, Berlin, Germany;
Departments of Dermatology and
Clinical Immunology, Charité, Humboldt University, Berlin, Germany; and
§
Department of Dermatology, University Hospital Eppendorf, University of Hamburg, Hamburg, Germany
Keratinocytes (KC) are important source of and targets for several
cytokines. Although KC express IL-15 mRNA, the functional effects of
IL-15 on these epithelial cells remain to be dissected. Investigating
primary human foreskin KC and HaCaT cells, we show here by
semiquantitative RT-PCR and flow cytometric analysis that both
translate IL-15 and IL-15R mRNA and express IL-15 and IL-15R
protein
on the cell surface, suggesting that human KC can employ IL-15 for
juxtacrine signaling. While IL-15 exerted no significant effect on KC
proliferation and IL-6 or IL-8 secretion, IL-15 inhibited both
anti-Fas and methylcellulose-induced KC apoptosis in vitro. This is
in line with the recognized potent anti-apoptotic effects of IL-15.
IL-2, whose receptor shares two components with the IL-15R, failed to
inhibit KC apoptosis. Together with the role of IL-15 in sustaining
chronic immune reactions, this invited the question of whether a
reduction of KC apoptosis by IL-15 may be involved in the pathogenesis
of psoriasis, a chronic hyperproliferative inflammatory skin disease
characterized by abnormally low KC apoptosis in the epidermis.
Remarkably, compared with nonlesional psoriatic skin and skin of
healthy volunteers, lesional psoriatic epidermis showed high IL-15
protein expression in the epidermis and enhanced binding activity for
IL-15. Therefore, antagonizing the inhibitory effects of IL-15 on KC
apoptosis deserves exploration as a novel therapeutic strategy in
psoriasis management.
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