International Immunology, Vol 9, 1423-1430, Copyright © 1997 by Oxford University Press
I Arsov and S Vukmanovic
The primary role of CD8+ T cells is to destroy virus-infected or tumor
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 mature,
H-Y/Db-specific CD8+ T cells from H-Y TCR transgenic mice were unable to
efficiently release lytic mediators after antigenic stimulation. However,
anti-TCR antibody induced granule exocytosis and target cell lysis, arguing
against signaling and/or cytolytic machinery defects in CD8+ cells, and
demonstrating that male antigen induced differentiation of 'naive' into
effector CD8+ cells. Stimulation of H-Y- specific effector CD8+ T cells
with male stimulators, although insufficient to induce lytic granule
release, was sufficient for H-Y- specific IFN-gamma production.
Unexpectedly, this effector-phase IFN- gamma production was dependent on
B7-2 engagement. We hypothesize that altered effector functions in
H-Y-specific CD8+ cells are due to the low affinity of TCR-antigen-MHC
interaction and/or the elevated threshold of CD8+ T cell activation.
ARTICLES
Altered effector responses of H-Y transgenic CD8+ cells
Michael Heidelberger Division of Immunology, Department of Pathology, NYU Medical Center, NY 10016, USA.
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