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The Journal of Immunology, 2004, 172: 2201-2209.
Copyright © 2004 by The American Association of Immunologists

IL-10-Conditioned Dendritic Cells, Decommissioned for Recruitment of Adaptive Immunity, Elicit Innate Inflammatory Gene Products in Response to Danger Signals1

Kathleen F. Nolan2,*, Victoria Strong*, Dulce Soler{dagger}, Paul J. Fairchild*, Stephen P. Cobbold*, Ruth Croxton*, Jose-Angel Gonzalo{dagger}, Ana Rubio{dagger}, Meghan Wells{dagger} and Herman Waldmann*

* Sir William Dunn School of Pathology, Oxford University, Oxford, United Kingdom; and {dagger} Millennium Pharmaceuticals, Cambridge, MA 02139

Dendritic cells (DCs) are the professional APCs of the immune system, enabling T cells to perceive and respond appropriately to potentially dangerous microbes, while also being able to maintain T cell tolerance toward self. In part, such tolerance can be determined by IL-10 released from certain types of regulatory T cells. IL-10 has previously been shown to render DCs unable to activate T cells and it has been assumed that this process represents a general block in maturation. Using serial analysis of gene expression, we show that IL-10 pretreatment of murine bone marrow-derived DCs alone causes significant changes in gene expression. Furthermore, these cells retain the ability to respond to Toll-like receptor agonists, but in a manner skewed toward the selective induction of mediators known to enhance local inflammation and innate immunity, among which we highlight a novel CXCR2 ligand, DC inflammatory protein-1. These data suggest that, while the presence of a protolerogenic and purportedly anti-inflammatory agent such as IL-10 precludes DCs from acquiring their potential as initiators of adaptive immunity, their ability to act as initiators of innate immunity in response to Toll-like receptor signaling is enhanced.




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