Pneumologie 2015; 69 - P463
DOI: 10.1055/s-0035-1544859

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

A Rabes 1, S Zimmermann 2, K Reppe 1, R Lang 3, PH Seeberger 4, N Suttorp 1, M Witzenrath 1, B Lepenies 2, B Opitz 1
  • 1Department of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité Universitätsmedizin Berlin
  • 2Max Planck Institute of Colloids and Interfaces, Department of Biomolecular Systems, Potsdam; Freie Universität Berlin, Institute of Chemistry and Biochemistry, Department of Biology, Chemistry and Pharmacy
  • 3Institute for Clinical Microbiology, Immunology and Hygiene, University Hospital Erlangen
  • 4Max Planck Institute of Colloids and Interfaces, Department of Biomolecular Systems, Potsdam

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 examined the function of Mincle in Streptococcus pneumoniae infection. Binding studies using a CLR library indicated a specific, Ca2+-dependent binding of Mincle to S. pneumoniae. 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. pneumoniae but is not required for the anti-pneumococcal innate immune response.