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*
Laboratory of Immunology, Istituto Dermopatico dell’Immacolata, IRCCS, Rome, Italy; and
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy
We have investigated the chemokine receptor expression and
migratory behavior of a new subset of nickel-specific skin-homing
regulatory CD4+ T cells (ThIL-10) releasing
high levels of IL-10, low IFN-
, and undetectable IL-4. These cells
inhibit in a IL-10-dependent manner the capacity of dendritic cells to
activate nickel-specific Tc1 and Th1 lymphocytes. RNase protection
assay and FACS analysis revealed the expression of a vast repertoire of
chemokine receptors on resting ThIL-10, including the
Th1-associated CXCR3 and CCR5, and the Th2-associated CCR3, CCR4, and
CCR8, the latter at higher levels compared with Th2 cells. The most
active chemokines for resting ThIL-10, in terms of calcium
mobilization and in vitro migration, were in order of potency: CCL2
(monocyte chemoattractant protein-1, CCR2 ligand), CCL4
(macrophage-inflammatory protein-1
, CCR5 ligand), CCL3
(macrophage-inflammatory protein-1
, CCR1/5 ligand), CCL17 (thymus
and activation-regulated chemokine, CCR4 ligand), CCL1 (I-309, CCR8
ligand), CXCL12 (stromal-derived factor-1, CXCR4), and CCL11 (eotaxin,
CCR3 ligand). Consistent with receptor expression down-regulation,
activated ThIL-10 exhibited a reduced or absent response to
most chemokines, but retained a significant migratory capacity to
I-309, monocyte chemoattractant protein-1, and thymus and
activation-regulated chemokine. I-309, which was ineffective on Th1
lymphocytes, attracted more efficiently ThIL-10 than Th2
cells. I-309 and CCR8 mRNAs were not detected in unaffected skin and
were up-regulated at the skin site of nickel-allergic reaction, with an
earlier expression kinetics compared with IL-10 and IL-4. Results
indicate that skin-homing regulatory ThIL-10 lymphocytes
coexpress functional Th1- and Th2-associated chemokine receptors, and
that CCR8/I-309-driven recruitment of both resting and activated
ThIL-10 cells may be critically involved in the regulation
of Th1-mediated skin allergic disorders.
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