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Department of Ophthalmology, Pathology, and Winship Cancer Center, Emory University School of Medicine, Atlanta, GA 30322
We previously reported that insulin-specific, MHC class
I-restricted CTL precursors can be primed by injecting C57BL/6 mice
with bovine insulin in CFA. These bovine insulin-primed CTL displayed a
type 0 CTL phenotype, producing IL-4, IL-5, IL-10, low levels of
IFN-
, but no TNF-
. By contrast, CTL generated from C57BL/6 mice
primed with OVA in CFA produced IFN- and TNF- but no IL-4, IL-5,
or IL-10 and therefore were classified as type 1 CTL. Although
CD4+ T cell subsets have been compared extensively in the
literature, CTL subsets are less well characterized. Here, the
phenotype, function, and requirements for the in vivo activation of
type 1 and type 0 CTL cells were studied. Although both types of CTL
express many of the same cell-surface Ags, OVA-specific CTL but not
bovine insulin-primed CTL expressed CT-1, a carbohydrate epitope of
CD45, and bovine insulin-primed CTL but not OVA-specific CTL expressed
Fas constitutively. Priming of CTL was abrogated by depletion of
phagocytic cells but not CD4+ T cells, whereas depletion of
CD4+ T cells but not phagocytic cells inhibited Ab
responses in the same mice. Neither endogenous IL-4 nor the dose of
priming Ag altered the CTL phenotypes, but the antigenic peptides of
OVA and bovine insulin were key to determining the differentiation of
either type 1 or type 0 CTL. To our knowledge, this is the first time
that antigenic epitopes have been demonstrated to influence the
phenotype of Ag-specific CTL responses. These results may be relevant
to the development of peptide vaccines in which a particular type of
CTL response is desired.
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