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*
Division of Dermatology, Sunnybrook and Women’s College Health Science Centre, and
Amgen Institute, Departments of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario, Canada; and
Department of Dermatology, University of Tsukuba, Tsukuba, Ibaraki, Japan
The role of CD4+ vs CD8+ T cells in contact
hypersensitivity (CHS) remains controversial. In this study, we used
gene knockout (KO) mice deficient in CD4+ or
CD8+ T cells to directly address this issue. Mice lacking
either CD4+ or CD8+ T cells demonstrated
depressed CHS responses to dinitrofluorobenzene and oxazolone compared
with wild-type C57BL/6 mice. The depression of CHS was more significant
in CD8 KO mice than in CD4 KO mice. Furthermore, in vivo depletion of
either CD8+ T cells from CD4 KO mice or CD4+ T
cells from CD8 KO mice virtually abolished CHS responses. Lymph node
cells (LNCs) from hapten-sensitized CD4 and CD8 KO mice showed a
decreased capacity for transferring CHS. In vitro depletion of either
CD4+ T cells from CD8 KO LNCs or CD8+ T cells
from CD4 KO LNCs resulted in a complete loss of CHS transfer. LNCs from
CD4 and CD8 KO mice produced significant amounts of IFN-
, indicating
that both CD4+ and CD8+ T cells are able to
secrete IFN-. LNCs from CD8, but not CD4, KO mice were able to
produce IL-4 and IL-10, suggesting that IL-4 and IL-10 are mainly
derived from CD4+ T cells. Intracellular cytokine staining
of LNCs confirmed that IFN--positive cells consisted of
CD4+ (Th1) and CD8+ (type 1 cytotoxic T) T
cells, whereas IL-10-positive cells were exclusively CD4+
(Th2) T cells. Collectively, these results suggest that both
CD4+ Th1 and CD8+ type 1 cytotoxic T cells are
crucial effector cells in CHS responses to dinitrofluorobenzene and
oxazolone in C57BL/6 mice.
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