Wednesday, February 3, 2016

Borrelia burgdorferi BBK32 Inhibits the Classical Pathway...

Pretty technical, but if biology is up your alley…

Author Summary

The human complement system is a connected network of blood proteins capable of recognizing and eliminating microbial intruders. To avoid the destructive force of complement activation, many microorganisms that enter the bloodstream express molecules that disrupt key steps of the complement cascade by interacting with specific complement components. In this study we show that the causative agent of Lyme disease, Borrelia burgdorferi, expresses a surface-protein termed BBK32 that targets and inhibits the first component of complement, designated C1.

Upon binding to human C1, BBK32 traps this initiating protease complex of the classical pathway of complement in an inactive state, and prevents the downstream proteolytic events of the pathway.

Our study defines a new mechanism by which microbes are able to escape the human innate immune system and identifies complement protease C1r as a previously unknown target of bacterial anti-complement molecules. Thus, discovery of the complement inhibitory activity of the borrelial protein BBK32 significantly advances our understanding of how disease-causing bacteria survive in immune competent hosts.

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