Up‐regulation of C5a receptor expression and function on human monocyte derived dendritic cells by prostaglandin E 2

• Published in: Immunology Vol. 110; no. 4; pp. 458 - 465
• Main Authors: Weinmann, Oliver, Gutzmer, Ralf, Zwirner, Jörg, Wittmann, Miriam, Langer, Katja, Lisewski, Margarete, Mommert, Susanne, Kapp, Alexander, Werfel, Thomas
• Format: Journal Article
• Language: English
• Published: 01.12.2003
• ISSN: 0019-2805; 1365-2567
• DOI: 10.1111/j.1365-2567.2003.01764.x

Summary 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‐α (TNF‐α), lipopolysaccharide (LPS) or CD40L and by the T helper 1‐cytokine interferon‐γ (INF‐γ). Prostaglandin E2 (PGE 2 ), 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‐α 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 PGE 2 . Stimulation of DC with C5a resulted in interleukin‐10 production which was significantly increased after C5aR up‐regulation with TNF‐α and PGE 2 . Therefore, up‐regulation of the C5aR on human DC alters their chemotactic and immunologic response to C5a.