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CUTTING EDGE |
*
Dermatology Branch, National Cancer Institute, Bethesda, MD 20892; and
Department of Dermatology, Emory University School of Medicine, Atlanta, GA 30322
Memory T cells (mTC) express multiple chemokine receptors
(including CCR4 and CCR6) that may potentially be involved in their
arrest on inflamed endothelia. Herein, we specifically addressed
whether CCR6 is required for mTC to arrest on TNF-
-activated human
dermal microvascular endothelial cells (HDMEC) in vitro under shear
stress conditions. Recombinant liver and activation-regulated chemokine
(LARC)/CCL20 (a CCR6 ligand) induced firm arrest of cutaneous
lymphocyte Ag+ mTC in a flow chamber system using purified
substrates. Strikingly, desensitization of CCR6 with LARC, but not
thymus and activation-regulated chemokine/CCL17 or secondary lymphoid
tissue chemokine/CCL21, caused a 50–75% decrease
(p < 0.001) in arrest of mTC on HDMEC, which was
indistinguishable from the reduction observed when total mTC were
treated with pertussis toxin (p > 0.5).
CCR6-depleted mTC also had a markedly reduced ability to arrest on
HDMEC. Our results suggest that LARC production by activated
endothelial cells and CCR6 expression by mTC may be critical components
in the pertussis toxin-sensitive arrest of mTC on activated
HDMEC.
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