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Blood, 1 February 2002, Vol. 99, No. 3, pp. 946-956
IMMUNOBIOLOGY
Immature mouse dendritic cells enter inflamed tissue, a process
that requires E- and P-selectin, but not P-selectin glycoprotein
ligand 1
Gunther G. Pendl,
Caroline Robert,
Meike Steinert,
Renate Thanos,
Ruth Eytner,
Eric Borges,
Martin K. Wild,
John B. Lowe,
Robert C. Fuhlbrigge,
Thomas S. Kupper,
Dietmar Vestweber, and
Stephan Grabbe
From the Institute of Cell Biology, ZMBE, and the
Department of Dermatology, University of Münster, Germany;
Harvard Skin Disease Research Center, Division of Dermatology, Brigham
and Women's Hospital, Harvard Institutes of Medicine, Boston, MA;
Department of Pathology, Howard Hughes Medical Institute,
University of Michigan Medical School, Ann Arbor; and Max Planck
Institute of Vascular Biology, Münster, Germany.
Inflammatory processes are associated with the rapid migration of
dendritic cells (DCs) to regional lymph nodes and depletion of these
potent antigen-presenting cells (APCs) from the inflamed tissue. This
study examined whether sites of cutaneous inflammation can be
repopulated with DCs from a pool of immature DCs circulating in the
blood. In adoptive transfer experiments with ex vivo-generated radioactively labeled primary bone marrow-derived DCs injected into
mice challenged by an allergic contact dermatitis reaction, immature
DCs were actively recruited from the blood to sites of cutaneous
inflammation, whereas mature DCs were not. Immature, but not mature,
DCs were able to adhere specifically to immobilized recombinant E- and
P-selectin under static as well as under flow conditions.
P-selectin-dependent adhesion of immature DCs correlates with their
higher level of expression of the carbohydrate epitope cutaneous
lymphocyte-associated antigen (CLA) and is blocked by a novel
inhibitory antibody against mouse P-selectin glycoprotein ligand 1 (PSGL-1). Surprisingly, however, emigration of immature DCs into
inflamed skin is retained in the presence of this anti-PSGL-1 antibody
and is also normal when immature DCs are generated from fucosyltransferase (Fuc-T) Fuc-TVII-deficient mice. By contrast, emigration of wild-type immature DCs is reduced by adhesion-blocking anti-E- and P-selectin antibodies, and immature DCs generated ex vivo
from Fuc-TVII/Fuc-TIV double-deficient mice emigrate poorly. Thus,
fucosylated ligands of the endothelial selectins, determined in part by
Fuc-TIV, and independent of PSGL-1, are required for extravasation of
DCs into sites of cutaneous inflammation.
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