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Department of Oncology (C6), Osaka University Graduate School of Medicine, Osaka, Japan
IL-12 was recently shown to induce CCR5 on TCR-triggered mouse T
cells. Considering that STAT4 is the most critical of IL-12 signaling
molecules, this study investigated the role for STAT4 in the induction
of CCR5 expression. IL-12R was induced by stimulation with anti-CD3
plus anti-CD28 mAb similarly on T cells from wild-type (WT) and
STAT4-deficient (STAT4-/-) mice, but the levels of IL-12R
induced on IFN-
-deficient (IFN--/-) T cells were
lower compared with WT T cells. Exposure of TCR-triggered WT T cells to
IL-12 induced CCR5 expression. In contrast, TCR-triggered
STAT4-/- T cells failed to express CCR5 in response to
IL-12. IL-12 stimulation induced detectable albeit reduced levels of
CCR5 expression on IFN--/- T cells. Addition of
rIFN- to cultures of IFN--/- T cells, particularly
to cultures during TCR triggering resulted in restoration of CCR5
expression. However, CCR5 expression was not induced in
STAT4-/- T cells by supplementation of rIFN-. These
results indicate that for the induction of CCR5 on T cells, 1) STAT4
plays an indispensable role; 2) such a role is not substituted by
simply supplementing rIFN-; and 3) IFN- amplifies CCR5 induction
depending on the presence of STAT4.
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