The primary role of CD8(+) T cells is to destroy virus-infected or tum
or cells expressing cognate antigens in the form of peptide-MHC class
I complexes. This destruction is primarily achieved by the actions of
lytic mediators and/or lymphokines. In this report, we show that matur
e, H-Y/D-b-specific CD8(+) T cells from H-Y TCR transgenic mice were u
nable to efficiently release lytic mediators after antigenic stimulati
on, However, anti-TCR antibody induced granule exocytosis and target c
ell lysis, arguing against signaling and/or cytolytic machinery defect
s in CD8(+) cells, and demonstrating that male antigen induced differe
ntiation of 'naive' into effector CD8(+) cells, Stimulation of H-Y-spe
cific effector CD8(+) T cells with male stimulators, although insuffic
ient to induce lytic granule release, was sufficient for H-Y-specific
IFN-gamma production, Unexpectedly, this effector-phase IFN-gamma prod
uction was dependent on B7-2 engagement, We hypothesize that altered e
ffector functions in H-Y-specific CD8(+) cells are due to the low affi
nity of TCR-antigen-MHC interaction and/or the elevated threshold of C
D8(+) T cell activation.