How the pathogen Staphylococcus aureus, a leading cause of hospital-related infections, disables the immune system is described online in Nature Immunology.
Defense against S. aureus infection requires immune molecules called complement proteins, which circulate in the bloodstream as inactive precursors. After complement proteins recognize and attach to invading microbes, they are clipped to smaller subunits, ultimately releasing end products that recruit more immune cells and trigger other defense mechanisms.
S. aureus produces a protein called Efb, which can somehow suppress complement function. Brian Geisbrecht and colleagues have now solved the structure of Efb, both alone and when bound to a complement protein. Their findings indicate that Efb binding alters the shape of complement proteins, thereby blocking the activating cleavage steps and subsequent formation of the antimicrobial complement complexes and release of inflammatory mediators. This work might be useful in designing methods to inhibit complement activation, which may be used as therapy for diseases involving excessive inflammation.
Brian Geisbrecht (University of Missouri-Kansas City, Kansas City, MO, USA)
Abstract available online.
(C) Nature Immunology press release.
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