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and TNF-
1
Laboratory of Immunology, Istituto Dermopatico dell’Immacolata, IRCCS, Rome, Italy
IL-17 is a novel T cell-derived cytokine that can regulate the
functions of a variety of cell types. In this study, we investigated
whether hapten-specific T cells isolated from patients with allergic
contact dermatitis (ACD) to nickel produce IL-17 and the effects of
IL-17 alone or in combination with IFN-
or TNF-
on the immune
activation of keratinocytes. Skin affected with ACD to nickel and
skin-derived, nickel-specific CD4+ T cell lines expressed
IFN-, TNF-, and IL-17 mRNAs. Four of seven nickel-specific
CD4+ T cell clones positive for the skin-homing receptor,
cutaneous lymphocyte-associated Ag, were shown to corelease IL-17,
IFN-, and TNF-. In contrast, two nickel-specific CD8+
T cell clones failed to synthesize IL-17. Normal human keratinocytes
were found to express constitutively the IL-17 receptor gene. IL-17
specifically and dose-dependently augmented IFN--induced ICAM-1
expression on keratinocytes at both the mRNA and the protein level,
whereas HLA-DR, MHC class I, and CD40 levels were not modulated by
IL-17. On the other hand, IL-17 alone did not affect ICAM-1 or
enhance TNF--induced ICAM-1. In addition, IL-17, both
directly and in synergism with IFN- and/or TNF-, stimulated
synthesis and release of IL-8 by keratinocytes. In contrast, IFN--
and TNF--induced production of RANTES was markedly inhibited by
IL-17, and the synthesis of macrophage chemotactic protein 1 was not
changed. Taken together, the results suggest that IL-17 is an important
player of T cell-mediated skin immune responses, with synergistic or
antagonist effects on IFN-- and TNF--stimulated keratinocyte
activation.
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