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The C-type lectin receptor Mincle binds to Streptococcus pneumoniae but plays a limited tole in the anti-pneumococcal innate immune response

MPG-Autoren
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Zimmermann,  Stephanie
Bernd Lepenies, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Seeberger,  Peter H.
Peter H. Seeberger - Vaccine Development, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Lepenies,  Bernd
Bernd Lepenies, Biomolekulare Systeme, Max Planck Institute of Colloids and Interfaces, Max Planck Society;

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Zitation

Rabes, A., Zimmermann, S., Reppe, K., Lang, R., Seeberger, P. H., Suttorp, N., et al. (2015). The C-type lectin receptor Mincle binds to Streptococcus pneumoniae but plays a limited tole in the anti-pneumococcal innate immune response. PLoS One, 10(2): e0117022. doi:10.1371/journal.pone.0117022.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0026-BFF8-9
Zusammenfassung
The innate immune system employs C-type lectin receptors (CLRs) to recognize carbohydrate structures on pathogens and self-antigens. The Macrophage-inducible C-type lectin (Mincle) is a FcRγ-coupled CLR that was shown to bind to mycobacterial cord factor as well as certain fungal species. However, since CLR functions during bacterial infections have not yet been investigated thoroughly, we aimed to examine their function in Streptococcus pneumonia infection. Binding studies using a library of recombinantly expressed CLR-Fc fusion proteins indicated a specific, Ca2+-dependent, and serotype-specific binding of Mincle to S. pneumonia. Subsequent experiments with different Mincle-expressing cells as well as Mincle-deficient mice, however, revealed a limited role of this receptor in bacterial phagocytosis, neutrophil-mediated killing, cytokine production, and antibacterial immune response during pneumonia. Collectively, our results indicate that Mincle is able to recognize S. pneumonia but is not required for the anti-pneumococcal innate immune response.