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*
Baylor Institute for Immunology Research, Dallas, TX 75204; and
Institut Paris-Sud Sur Les Cytokines, Institut National de la Santé et de la Recherche Médicale, Clamart, France
Monocyte-derived dendritic cells (MDDCs) activate naive T
lymphocytes to induce adaptive immunity, effecting Th1 polarization
through IL-12. However, little is known about other potential DC Th1
polarizing mechanisms, or how T cell polarization may be affected by
DCs differentiating in, or exposed to, a proinflammatory environment.
Macrophages (M
s) are DC precursors abundant in inflamed tissues,
lymph nodes, and tumors. Thus we studied the T cell-activating and
-polarizing properties of M-derived DCs (DCs). Monocytes were
cultured in M-CSF (M-CSF) to produce Ms, which were then
differentiated into DCs following culture with GM-CSF plus IL-4. DCs
activated a significant allogeneic MLR and were significantly better
than MDDCs in activating T cells with superantigen. Most strikingly,
DCs elicited up to 9-fold more IFN-
from naive or Ag-specific T
cells compared with MDDCs (with equivalent IL-4 secretion), despite
producing up to 9-fold less IL-12. Neutralization of MDDC, but not
DC IL-12 significantly inhibited T cell IFN- induction. DCs
produced up to 12-fold more ß-chemokines (macrophage-inflammatory
protein-1
, -1ß, and RANTES) than MDDCs. Ab blockade of CCR5, but
not CXC chemokine receptor 4, inhibited T cell IFN- induction by
DCs significantly greater than by MDDCs. Thus DCs differentiating
from Ms induce T cell IFN- through ß-chemokines with little or
no requirement for IL-12. Myeloid DCs arising from distinct precursor
cells may have differing properties, including different mechanisms of
Th1 polarization. These data are the first reports of IFN- induction
through chemokines by DCs.
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