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PLoS One. 2015 Feb 6;10(2):e0117022. doi: 10.1371/journal.pone.0117022. eCollection 2015.

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

Author information

1
Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany.
2
Max Planck Institute of Colloids and Interfaces, Department of Biomolecular Systems, Potsdam, Germany; Freie Universität Berlin, Institute of Chemistry and Biochemistry, Department of Biology, Chemistry and Pharmacy, Berlin, Germany.
3
Institute for Clinical Microbiology, Immunology and Hygiene, University Hospital Erlangen, Erlangen, Germany.
4
Max Planck Institute of Colloids and Interfaces, Department of Biomolecular Systems, Potsdam, Germany.

Abstract

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.

PMID:
25658823
PMCID:
PMC4319728
DOI:
10.1371/journal.pone.0117022
[Indexed for MEDLINE]
Free PMC Article

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