Immune evasion by a staphylococcal complement inhibitor that acts on C3 convertases

Suzan H.M. Rooijakkers*, Maartje Ruyken, Anja Roos, Mohamed R. Daha, Julia S. Presanis, Robert B. Sim, Willem J.B. van Wamel, Kok P.M. van Kessel, Jos A.G. van Strijp

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

343 Citations (Scopus)


The complement system is pivotal in host defense but also contributes to tissue injury in several diseases. The assembly of C3 convertases (C4b2a and C3bBb) is a prerequisite for complement activation. The convertases catalyze C3b deposition on activator surfaces. Here we describe the identification of staphylococcal complement inhibitor, an excreted 9.8-kilodalton protein that blocks human complement by specific interaction with C4b2a and C3bBb. Staphylococcal complement inhibitor bound and stabilized C3 convertases, interfering with additional C3b deposition through the classical, lectin and alternative complement pathways. This led to a substantial decrease in phagocytosis and killing of Staphylococcus aureus by human neutrophils. As a highly active and small soluble protein that acts exclusively on surfaces, staphylococcal complement inhibitor may represent a promising anti-inflammatory molecule.

Original languageEnglish
Pages (from-to)920-927
Number of pages8
JournalNature Immunology
Issue number9
Publication statusPublished - Sept 2005
Externally publishedYes

Bibliographical note

Funding Information:
We thank W. Jansen for reviewing the manuscript, and L. de Graaf-Miltenburg for purification of factor B and C3. Supported by the European Union (LSHM-CT-2004-512093 and QLG1-CT-2001-01039).


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