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Molecular mechanisms of complement evasion: learning from staphylococci and meningococci

Abstract

The complement system is a crucial component of the innate immune response in humans. Recent studies in Staphylococcus aureus and Neisseria meningitidis have revealed how these bacteria escape complement-mediated killing. In addition, new structural data have provided detailed insights into the molecular mechanisms of host defence mediated by the complement system and how bacterial proteins interfere with this process. This information is fundamental to our understanding of bacterial pathogenesis and may facilitate the design of better vaccines.

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Figure 1: The complement system and selected bacterial inhibitors.
Figure 2: The available structural data for the alternative pathway.
Figure 3: Structures of bacterial proteins that bind complement components and of their complexes with complement proteins.

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Acknowledgements

The authors thank M. Pizza and F. Bagnoli for critical reading of the manuscript. P.G. acknowledges the members of his research group, and financial support from the Council for Chemical Sciences of the Netherlands Organization for Scientific Research and the US National Institutes of Health.

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Correspondence to Rino Rappuoli.

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Davide Serruto, Rino Rappuoli, Maria Scarselli, Piet Gros & Jos A. G. van Strijp.

Molecular mechanisms of complement evasion: learning from staphylococci and meningococci. Nature Reviews Microbiology 8, 393–399 (2010); doi:10.1038/nrmicro2366

Davide Serruto, Rino Rappuoli and Maria Scarselli are employed by Novartis Vaccines and Diagnostics.

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DATABASES

Entrez Genome Project

Bordetella pertussis

Borrelia burgdorferi

group A Streptococcus

group B Streptococcus

Neisseria meningitidis

Staphylococcus aureus

Streptococcus pneumoniae

Yersinia enterocolitica

Protein Data Bank

2GOM

2GOX

2KC0

2NOJ

2QFF

2W80

2WIN

3KLS

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Serruto, D., Rappuoli, R., Scarselli, M. et al. Molecular mechanisms of complement evasion: learning from staphylococci and meningococci. Nat Rev Microbiol 8, 393–399 (2010). https://doi.org/10.1038/nrmicro2366

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