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Laboratory of Cellular and Clinical Immunology, Institut National de la Santé et de la Recherche Médicale Unité 255, Institut de Recherches Biomédicales des Cordeliers, Paris, France; and
Schering-Plough, Laboratory for Immunological Research, Dardilly, France
Immune responses are initiated by dendritic cells (DC) that form a
network comprising different populations. In particular, Langerhans
cells (LC) appear as a unique population of cells colonizing epithelial
surfaces. We have recently shown that macrophage-inflammatory
protein-3
/CCL20, a chemokine secreted by epithelial cells, induces
the selective migration of LC among DC populations. In this study, we
investigated the effects of cytokines on the expression of the CCL20
receptor, CCR6, during differentiation of LC. We found that both IL-4
and IFN-
blocked the expression of CCR6 and CCL20 responsiveness at
different stages of LC development. The effect of IL-4 was reversible
and most likely due to the transient blockade of LC differentiation. In
contrast, IFN--induced CCR6 loss was irreversible and was
concomitant to the induction of DC maturation. When other cytokines
involved in DC and T cell differentiation were tested, we found that
IL-10, unlike IL-4 and IFN-, maintained CCR6 expression. The effect
of IL-10 was reversible and upon IL-10 withdrawn, CCR6 was lost
concomitantly to final LC differentiation. In addition, IL-10 induced
the expression of CCR6 and responsiveness to CCL20 in differentiated
monocytes that preserve their ability to differentiate into mature DC.
Finally, TGF-
, which induces LC differentiation, did not alter early
CCR6 expression, but triggered its irreversible down-regulation, in
parallel to terminal LC differentiation. Taken together, these results
suggest that the recruitment of LC at epithelial surface might be
suppressed during Th1 and Th2 immune responses, and amplified during
regulatory immune responses involving IL-10 and
TGF-.
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