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*
Laboratory of Tumor Immunology, Scientific Institute San Raffaele, Milan, Italy;
Laboratory of Pathology, Scientific Institute San Raffaele, Milan, Italy; and
Laboratory of Immunopathology, National Institute for Cancer Research and Advanced Biotechnology Center (IST-CBA), Genoa, Italy
We describe a subset of peripheral CD14+ cells,
coexpressing the CD34 progenitor marker and able to migrate across
endothelial cell monolayers. On culture with
granulocyte-macrophage-CSF, this population differentiated into
dendritic cells expressing CD83, CD80, HLA-DRbright, CD86,
and CD54. These dendritic cells were immunostimulatory, in that they
induced proliferation of allogenic and tetanus toxoid-specific T
lymphocytes. The CD14+CD34+ population
expressed higher levels of platelet endothelial cell adhesion
molecule-1 (PECAM-1) and 
4ß1 integrin than
the CD14+CD34- counterpart, being dull
positive for other integrins. Using stably transfected
PECAM-1+, VCAM-1+, or ICAM-1+
cells, we found that PECAM-1 and, to a lesser extent, VCAM-1, could
support transmigration of CD14+CD34+ cells,
whereas the L-ICAM-1 interaction was involved in cell adhesion.
PECAM-1-driven transmigration was conceivably dependent on a
haptotactic gradient, as it was reduced by 80% across NIH/3T3 cells
transfected with the PECAM-1-
cyto deletion mutant. This mutant lacks
the cytoplasmic tail and displays a reduced tendency to localize at the
intercellular junctions, thus failing to form a molecular junctional
gradient. Once differentiated, dendritic cells derived from
CD14+CD34+ precursors retained their
transendothelial migratory capability, using both PECAM-1 and ICAM-1
for transmigration. We suggest that a subset of
CD14+CD34+ circulating leukocytes can localize
to peripheral tissues and differentiate into functional dendritic
cells, thus representing a functional reservoir of potential APC.
PECAM-1, constitutively expressed on vascular endothelium, is likely to
play a relevant role in the egress of this population from the
bloodstream.
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