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*
Division of Dermatology and
Pulmonary Medicine,
Department of Microbiology and Immunology, and Molecular Biology Institute, University of California School of Medicine, Los Angeles, CA 90095;
§
Genentech Incorporated, South San Francisco, CA 94080; and
¶
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75235
The ability of dendritic cells (DC) to initiate immune responses in
naive T cells is dependent upon a maturation process that allows the
cells to develop their potent Ag-presenting capacity. Although immature
DC can be derived in vitro by treatment of peripheral blood monocytes
with GM-CSF and IL-4, additional signals such as those provided by
TNF-
, CD40 ligand, or LPS are required for complete maturation and
maximum APC function. Because we recently found that microbial
lipoproteins can activate monocytes and DC through Toll-like receptor
(TLR) 2, we also investigated whether lipoproteins can drive DC
maturation. Immature DC were cultured with or without lipoproteins and
were monitored for expression of cell surface markers indicative of
maturation. Stimulation with lipopeptides increased expression of CD83,
MHC class II, CD80, CD86, CD54, and CD58, and decreased CD32 expression
and endocytic activity; these lipopeptide-matured DC also displayed
enhanced T cell stimulatory capacity in MLR, as measured by T cell
proliferation and IFN-
secretion. The lipid moiety of the
lipopeptide was found to be essential for induction of maturation.
Preincubation of maturing DC with an anti-TLR2 blocking Ab before
addition of lipopeptide blocked the phenotypic and functional changes
associated with DC maturation. These results demonstrate that
lipopeptides can stimulate DC maturation via TLR2, providing a
mechanism by which products of bacteria can participate in the
initiation of an immune response.
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