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Department of Oncology, Biomedical Research Center, Osaka University Graduate School of Medicine, Yamada-oka, Suita, Osaka, Japan
CD5 positively costimulates TCR-stimulated mature T cells, whereas
this molecule has been suggested to negatively regulate the activation
of TCR-triggered thymocytes. We investigated the effect of CD5
costimulation on the differentiation of
CD4+CD8+ thymocytes. Coligation of thymocytes
with anti-CD3 and anti-CD5 induced enhanced tyrosine
phosphorylation of LAT (linker for activation of T cells) and
phospholipase C-
(PLC-) compared with ligation with anti-CD3
alone. Despite increased phosphorylation of PLC-, this treatment
down-regulated Ca2+ influx. In contrast, the
phosphorylation of LAT and enhanced association with Grb2 led to
activation of extracellular signal-regulated kinase (ERK)
mitogen-activated protein kinase. When CD3 and CD5 on
CD4+CD8+ thymocytes in culture were coligated,
they lost CD8, down-regulated CD4 expression, and induced CD69
expression, yielding a
CD4+(dull)CD8-CD69+ population. An
ERK inhibitor, PD98059, inhibited the generation of this population.
The reduction of generation of CD4+CD8- cells
resulted from decreased survival of these differentiating thymocytes.
Consistent with this, PD98059 inhibited the anti-CD3/CD5-mediated
Bcl-2 induction. These results indicate that CD5 down-regulates a
branch of TCR signaling, whereas this molecule functions to support the
differentiation of CD4+CD8+ thymocytes by
up-regulating another branch of TCR signaling that leads to ERK
activation.
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