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Institut National de la Santé et de la Recherche Médicale,
*
Unité 503 and
Unité 404, Lyon, France; and
Department of Dermatology, Fukushima Medical University School of Medicine, Fukushima, Japan
Contact hypersensitivity (CHS) is a T cell-mediated, Ag-specific
skin inflammation induced by skin exposure to haptens in sensitized
individuals. Th1/T cytotoxic 1 cells are effector cells of CHS, whereas
Th2/T regulatory CD4+ T cells have down-regulating
properties. We have previously shown that CHS to
2,4-dinitrofluorobenzene is mediated by specific CD8+
effector cells, whose cytolytic activity is mandatory for induction of
skin inflammation. In this study, using immunohistochemistry and RT-PCR
analysis, we show that CD8+ T cells are rapidly recruited
into the skin at the site of hapten challenge before the onset of
clinical and histological signs of skin inflammation. This early
CD8+ T cell recruitment is concomitant with: 1) transient
IFN-
mRNA expression suggesting local activation of effector cells;
and 2) induction of keratinocyte (KC) apoptosis which gradually
increased to a maximum at the peak of the CHS response. Alternatively,
skin infiltration of CD4+ T cells occurred later and
coincided with the peak of the CHS reaction and the beginning of the
resolution of skin inflammation. Mice deficient in CD8+ T
cells did not develop CHS, whereas mice deficient in CD4+ T
cells developed an enhanced inflammatory response with increased
numbers of CD8+ T cells recruited in the skin associated
with massive KC apoptosis. These data show that CHS is due to the early
and selective recruitment in the skin of CD8+ T cytotoxic 1
effector cells responsible for KC apoptosis.
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