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Chemokine Biology Laboratory, Department of Molecular Biosciences, Adelaide University, Adelaide, Australia
Following infection, naive T cells are activated in the secondary
lymphoid tissue, but then need to move to the infected tissue in the
periphery to mediate their effector functions. The acquisition of
inflammatory chemokine receptors, such as CCR5 and CCR6, may contribute
to the efficient relocation of activated T cells to inflamed sites in
the periphery. In keeping with this idea, the present study has
demonstrated that CCR5 and CCR6 are up-regulated on CD4+ T
cells upon activation in the MLR. The observed increase in expression
correlated well with the acquisition of an activated/memory phenotype
and was largely (CCR5) or completely (CCR6) separated temporally from
the initiation of cell division. In contrast, the regulation of two
other chemokine receptors, CXCR3 and CXCR4, occurred in close parallel
with the cell division process. Increased mRNA levels are likely to
contribute to the enhanced surface expression of CCR5 and CCR6, but in
the case of CCR6, translocation of intracellular stores of protein to
the cell surface may be an additional mechanism of regulation. The
up-regulation of CCR5 was more extensive than that of CCR6, as only
approximately half the activated CCR5+ T cells coexpressed
CCR6. The increased expression of CCR5 resulted in enhanced chemotaxis
toward the CCR5 ligand macrophage-inflammatory protein-1
/CCL4, but
up-regulation of CCR6 did not result in altered chemotactic
responsiveness to macrophage-inflammatory protein-3
/CCL20,
suggesting an alternative function for this
receptor.
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