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IL-10-conditioned dendritic cells, decommissioned for recruitment of adaptive immunity, elicit innate inflammatory gene products in response to danger signals
Nolan, K F; Strong, V; Soler, D; Fairchild, P J; Cobbold, S P; Croxton, R; Gonzalo, J A; Rubio, A; Wells, M; Waldmann, H
J Immunol. 2004;172(4):2201-9.
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Abstract
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.
Keyword(s)
Amino Acid Motifs; Animals; Bone Marrow Cells/immunology/metabolism; Cell Differentiation/genetics/immunology; Cell Line; Cell Line, Tumor; Cell Movement/genetics/*immunology; Cells, Cultured; Chemokines, CXC/antagonists & inhibitors/biosynthesis/genetics/physiology; Chemotaxis, Leukocyte/immunology; Dendritic Cells/cytology/*immunology/*metabolism; Gene Expression Regulation/*immunology; Gene Library; Humans; Immunity, Innate/genetics; Inflammation Mediators/*metabolism; Interleukin-10/*physiology; Lipopolysaccharides/pharmacology; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred CBA; Molecular Sequence Data; Monomeric GTP-Binding Proteins/antagonists &; Neutrophil Infiltration/immunology; Nucleic Acid Amplification Techniques; RNA, Messenger/biosynthesis; Receptors, Interleukin-8B/physiology; inhibitors/*biosynthesis/*genetics/physiology
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