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Staphylococcus aureus wall teichoic acid is a pathogen-associated molecular pattern that is recognized by langerin (CD207) on skin Langerhans cells

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Fuchsberger,  Felix F.
Christoph Rademacher, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Hanske,  Jonas
Christoph Rademacher, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Rademacher,  Christoph
Christoph Rademacher, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Citation

van Dalen, R., De La Cruz Diaz, J. S., Rumpret, M., Fuchsberger, F. F., van Teijlingen, N. H., Hanske, J., et al. (2017). Staphylococcus aureus wall teichoic acid is a pathogen-associated molecular pattern that is recognized by langerin (CD207) on skin Langerhans cells. bioRxiv. doi:10.1101/238469.


Cite as: http://hdl.handle.net/21.11116/0000-0001-AAB0-8
Abstract
Staphylococcus aureus is a major cause of skin and soft tissue infections and aggravator of the inflammatory skin disease atopic dermatitis (AD). Langerhans cells (LCs) initiate a Th17 response upon exposure to S. aureus, which contributes to host defense but also to AD pathogenesis. However, the molecular mechanisms underlying the unique pro-inflammatory capacities of S. aureus remain unclear. We demonstrate that human LCs directly interact with S. aureus through the pattern-recognition receptor langerin (CD207), which specifically recognizes the conserved β-N-acetylglucosamine (GlcNAc) modifications of wall teichoic acid (WTA) that are not expressed by other staphylococcal species. The WTA glycoprofile strongly influences the production of Th1- and Th17-polarizing cytokines by LCs. Specifically, β-GlcNAc activates LCs, whereas co-decoration of WTA with α-GlcNAc through the enzyme TarM, uniformly present in the AD-associated CC1 lineage, attenuates LC immune activation. Our findings provide important mechanistic insights into the role of S. aureus in inflammatory skin disease.