Abstract |
The expression of the C5a-receptor (C5aR) on dendritic cells, its regulation and function have not been well established thus far. We show that the C5aR is expressed on human monocyte-derived dendritic cells (DC) and can be down-regulated by maturation stimuli such as tumour necrosis factor-alpha ( TNF-alpha), lipopolysaccharide (LPS) or CD40L and by the T helper 1-cytokine interferon-gamma (INF-gamma). Prostaglandin E2 ( PGE2), a proinflammatory mediator supporting dendritic cell activation and necessary for adequate DC migration, leads to the up-regulation of C5aR expression when incubated alone and prevents down-regulation when given in combination with TNF-alpha or LPS. Stimulation of C5aR on DC triggered F-actin polymerization, indicating the chemotactic potential of DC elicited by C5a. C5a induced F-actin polymerization was increased when C5aR was up-regulated by PGE2. Stimulation of DC with C5a resulted in interleukin-10 production which was significantly increased after C5aR up-regulation with TNF-alpha and PGE2. Therefore, up-regulation of the C5aR on human DC alters their chemotactic and immunologic response to C5a.
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Authors | Oliver Weinmann, Ralf Gutzmer, Jörg Zwirner, Miriam Wittmann, Katja Langer, Margarete Lisewski, Susanne Mommert, Alexander Kapp, Thomas Werfel |
Journal | Immunology
(Immunology)
Vol. 110
Issue 4
Pg. 458-65
(Dec 2003)
ISSN: 0019-2805 [Print] England |
PMID | 14632643
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Actins
- CD40 Antigens
- Lipopolysaccharides
- Polymers
- Receptor, Anaphylatoxin C5a
- Tumor Necrosis Factor-alpha
- Interleukin-10
- Interferon-gamma
- Dinoprostone
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Topics |
- Actins
(immunology, metabolism)
- CD40 Antigens
(immunology)
- Dendritic Cells
(immunology)
- Dinoprostone
(immunology)
- Down-Regulation
(immunology)
- Flow Cytometry
(methods)
- Humans
- Interferon-gamma
(immunology)
- Interleukin-10
(biosynthesis, immunology)
- Lipopolysaccharides
(immunology)
- Monocytes
(immunology)
- Polymerase Chain Reaction
(methods)
- Polymers
(metabolism)
- Receptor, Anaphylatoxin C5a
(immunology)
- Tumor Necrosis Factor-alpha
(immunology)
- Up-Regulation
(immunology)
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