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-Induced Activation and Maturation of Human Peripheral Blood Monocyte-Derived Dendritic Cells
*
Department of Cell Processing, Institute of Medical Science, University of Tokyo, Tokyo, Japan; and
Japanese Red Cross Central Blood Center, Tokyo, Japan
TNF-
or IL-10 has been implicated to reversibly regulate
physiological states of dendritic cells (DCs). However, little is known
about dual stimulations of these cytokines on DC properties and the
intracellular signaling events that are responsible for the regulation
of these states. Here, we show that a family of mitogen-activated
protein kinases (MAPKs), extracellular signal-regulated kinase 2
(ERK2), stress-activated protein kinase/c-Jun N-terminal kinase
(SAPK/JNK), and p38mapk, are potentially
involved in IL-10-mediated selective suppression of TNF--induced
changes of the monocyte-derived DC properties. TNF- induced the
cluster formation of the cells and the enhancement of cell surface
expression levels of CD83, CD86, and HLA-DR, and T cell stimulatory
capacity, whereas the capacities for the endocytosis and the
chemotactic migration were suppressed in these cells. Treatment of
monocyte-derived DCs with IL-10 resulted in the reduction of the cell
surface expression levels of CD86, HLA-DR, and T cell stimulatory
capacity, whereas both endocytic and chemotactic migratory capacities
were increased by IL-10. Dual stimulations of monocyte-derived DCs with
TNF- and IL-10 selectively antagonized their respective effects on
these DC properties. TNF- induced tyrosine phosphorylation and
enzymatic activation of ERK2, SAPK/JNK, and
p38mapk, whereas IL-10 did not induce
these events. Dual stimulations of TNF- plus IL-10 abolished
TNF--induced changes of these MAPKs in DCs. These results suggest
that the blockage in the MAPKs cascades contributes to IL-10-mediated
repression of TNF--induced changes of DC
properties.
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