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Blood, 15 January 2002, Vol. 99, No. 2, pp. 600-608
IMMUNOBIOLOGY
Adenovirus type 5 vectors induce dendritic cell differentiation
in human CD14+ monocytes cultured under serum-free
conditions
Lyudmila A. Lyakh,
Gary K. Koski,
Howard A. Young,
Sally E. Spence,
Peter A. Cohen, and
Nancy R. Rice
From the Regulation of Cell Growth Laboratory, the
Laboratory of Experimental Immunology, and the Mouse Cancer Genetics
Program, National Cancer Institute at Frederick, MD, and the Center for
Surgery Research, Cleveland Clinic Foundation, OH.
To determine whether infection by a model virus is capable of
initiating dendritic cell (DC) differentiation, human CD14+
peripheral blood monocytes were infected with replication-defective type 5 adenovirus. Under serum-free conditions, this resulted in differentiation of a majority of cells toward a DC phenotype within
36 to 48 hours, without the need for cytokine-induced
predifferentiation. Infection induced DC morphology and altered the
expression of surface markers, including loss of CD14, de novo
induction of CD83 and CD25, and strongly augmented expression of CD86,
CD80, CD40, and HLA-DR and HLA class I molecules.
Differentiated cells maintained immunophenotype without loss of
viability for at least 2 days after removal of the differentiation
agent and cytokines. A greatly enhanced capacity to stimulate
T-lymphocyte alloproliferation and increased expression of the
DC-associated transcription factor RelB were observed. Virus without
transgene was found to induce changes similar to transgene-expressing
viruses. RelB up-regulation and DC immunophenotype were sensitive to
the antioxidant N-acetylcysteine, suggesting a critical
role for nuclear factor  B. RNAse protection assays revealed elevated
levels of messenger RNA for a number of chemokines and cytokines
associated with DCs. Finally, during differentiation,
adenovirus-infected monocytes were shown to secrete chemokines and
cytokines, including tumor necrosis factor- (TNF-). Furthermore,
a TNF--neutralizing antibody inhibited the expression of some DC
surface markers, indicating a contributing role for this cytokine in
the adenovirus-induced differentiation of DC from monocytes. These
findings have implications for the biology of monocytes as precursors
to DCs and also for the use of recombinant adenovirus in vaccines or
gene therapy.
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