Staphylococcal complement inhibitor modulates phagocyte responses by dimerization of convertases.

Journal article

The human pathogen Staphylococcus aureus produces several complement-evasion molecules that enable the bacterium to withstand the host immune response. The human-specific staphylococcal complement inhibitor (SCIN) blocks the central C3 convertase enzymes that trigger critical complement functions, such as C3b deposition, phagocytosis, and C5a generation. SCIN effectively blocks the conversion of C3 by alternative pathway C3 convertases (C3bBb), but also induces dimerization of these enzymes. ...

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Authors: Jongerius, I; Puister, M; Wu, J; Ruyken, M; van Strijp, J

• Journal: Journal of Immunology
• Volume: 184
• Issue: 1
• Pages: 420-425
• Publication date: 2010-01-01
• DOI: 10.4049/jimmunol.0902865
• EISSN: 1550-6606
• ISSN: 0022-1767
• Language: English
• Keywords: Humans; Staphylococcus aureus; Animals; Phagocytosis; Cricetulus; CHO Cells; Staphylococcal Infections; Cricetinae; Antigens, Bacterial; Dimerization; Complement C3; Electrophoresis, Polyacrylamide Gel; Complement C3-C5 Convertases