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*
Institut National de la Santé et de la Recherche Médicale Unite 454, Montpellier, France;
Laboratoire d’Immunologie des Infections Retrovirales, Institut de Biologie, Montpellier, France; and
Laboratoire de Virologie, Centre Hospitalier Universitaire St. Eloi, Montpellier, France
In the present study, we show that IL-2, IL-4, IL-7, and IL-15 are
able to induce functional CXCR4 surface expression on resting in
vitro-generated CD4+ CXCR4- CCR7+
memory T cells. Cytokine-mediated induction of CXCR4 expression was
associated with an increase in CXCR4 transcription, enhanced
stromal-derived factor-1-induced T cell migration in vitro, and
increased susceptibility of these cells to infection with X4 strains of
HIV-1. CXCR4 expression could also be induced through an alternative
pathway, following coculture of these cells with CD40-activated,
autologous, CD34+ progenitor-derived dendritic cells.
Although these dendritic cells express transcripts for IL-7 and IL-15,
addition of neutralizing anti-IL-7R and IL-15 mAbs did not block
induction of CXCR4 expression. Indeed, dendritic cell-mediated
up-regulation of CXCR4 expression was found to depend on CD40/CD154 and
CD134/CD134L interactions. Whereas activated autologous dendritic cells
induced the expression of both CXCR4 and CD25 on a portion of
CCR7+ memory T cells, concomitant CD3-mediated activation
of these cells further enhanced CD25 expression, but, in contrast,
prevented induction of CXCR4 expression. This observation suggests that
triggering of the CD134 and CD154 molecules, in contrast to TCR/CD3
complex-mediated stimulation, results in simultaneous T cell activation
and CXCR4 expression. Taken together, these results show that common
-chain-interacting cytokines as well as signals mediated via
noncognate interactions between activated dendritic cells and memory T
cells are involved in the up-regulation of CXCR4
expression.
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