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Blood, 15 November 2001, Vol. 98, No. 10, pp. 3022-3029
IMMUNOBIOLOGY
Expression of CCR-7, MIP-3 , and Th-1 chemokines in type I
IFN-induced monocyte-derived dendritic cells: importance for the rapid
acquisition of potent migratory and functional activities
Stefania Parlato,
Stefano
M. Santini,
Caterina Lapenta,
Tiziana Di
Pucchio,
Mariantonia Logozzi,
Massimo Spada,
Anna Maria Giammarioli,
Walter Malorni,
Stefano Fais, and
Filippo Belardelli
From the Laboratory of Virology, Laboratory of
Ultrastructures, and Laboratory of Immunology, Istituto Superiore di
Sanità, Rome, Italy.
The migration capability of dendritic cells (DCs) is regulated by
their response to factors, namely chemokines, that characterize maturation stage and shape their functional activities. This study examines the morphology, expression of chemokines/chemokine receptors, and migration properties of DCs generated after treatment of monocytes with type I interferon (IFN) and granulocyte-macrophage
colony-stimulating factor (GM-CSF) (IFN-DCs). IFN-DCs showed
phenotypical and morphologic features undetectable in DCs generated in
the presence of interleukin 4 (IL-4) and GM-CSF, such as
expression of CD83 and CD25 and the presence of CD44+,
highly polarized, thin, and long dendrites. IFN-DCs markedly migrated
in response to  -chemokines (especially MIP-1) and expressed the
Th-1 chemokine IP-10. Notably, IFN-DCs showed an up-regulation of CCR7
as well as of its natural ligand MIP-3, characteristics typical of
mature DCs. Of interest, IFN-DCs exhibited a marked chemotactic
response to MIP-3 in vitro and strong migratory behavior in severe
combined immunodeficient (SCID) mice. In SCID mice reconstituted with
human peripheral blood leukocytes, IFN-DCs induced a potent primary human antibody response and IFN- production, indicative of a
Th-1 immune response. These results define the highly specialized maturation state of IFN-DCs and point out the existence of a "natural alliance" between type I IFN and monocyte/DC development,
instrumental for ensuring an efficient connection between innate and
adaptive immunity.
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