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Enhances CD40 Ligand-Mediated Cytokine Secretion by Human Dendritic Cells (DC): A Mechanism for T Cell-Independent DC Activation1
*
Melbourne Tumor Biology Branch, Ludwig Institute for Cancer Research, Austin and Repatriation Medical Center, Heidelberg, Victoria, Australia;
University of Heidelberg, Heidelberg, Germany;
Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia; and
Immunex Corporation, Seattle, WA 98101
CD40 ligand (CD40L) is a membrane-bound molecule expressed by
activated T cells. CD40L potently induces dendritic cell (DC)
maturation and IL-12p70 secretion and plays a critical role during T
cell priming in the lymph nodes. IFN-
and IL-4 are required for
CD40L-mediated cytokine secretion, suggesting that T cells are required
for optimal CD40L activity. Because CD40L is rapidly up-regulated by
non-T cells during inflammation, CD40 stimulation may also be important
at the primary infection site. However, a role for T cells at the
earliest stages of infection is unclear. The present study demonstrates
that the innate immune cell-derived cytokine, IL-1
, can increase
CD40L-induced cytokine secretion by monocyte-derived DC,
CD34+-derived DC, and peripheral blood DC independently of
T cell-derived cytokines. Furthermore, IL-1 is constitutively
produced by monocyte-derived DC and monocytes, and is increased in
response to intact Escherichia coli or CD40L, whereas
neither CD34+-derived DC nor peripheral blood DC produce
IL-1. Finally, DC activated with CD40L and IL-1 induce higher
levels of IFN- secretion by T cells compared with DC activated with
CD40L alone. Therefore, IL-1 is the first non-T cell-derived
cytokine identified that enhances CD40L-mediated activation of DC. The
synergy between CD40L and IL-1 highlights a potent, T
cell-independent mechanism for DC activation during the earliest stages
of inflammatory responses.
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