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Proc Natl Acad Sci U S A. 2010 Oct 12;107(41):17621-6. doi: 10.1073/pnas.1003750107. Epub 2010 Sep 27.

Allosteric inhibition of complement function by a staphylococcal immune evasion protein.

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1
Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Abstract

The complement system is a major target of immune evasion by Staphylococcus aureus. Although many evasion proteins have been described, little is known about their molecular mechanisms of action. Here we demonstrate that the extracellular fibrinogen-binding protein (Efb) from S. aureus acts as an allosteric inhibitor by inducing conformational changes in complement fragment C3b that propagate across several domains and influence functional regions far distant from the Efb binding site. Most notably, the inhibitor impaired the interaction of C3b with complement factor B and, consequently, formation of the active C3 convertase. As this enzyme complex is critical for both activation and amplification of the complement response, its allosteric inhibition likely represents a fundamental contribution to the overall immune evasion strategy of S. aureus.

PMID:
20876141
PMCID:
PMC2955122
DOI:
10.1073/pnas.1003750107
[Indexed for MEDLINE]
Free PMC Article

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