Human genetic deficiencies reveal the roles of complement in the inflammatory network: lessons from nature.

ABSTRACT: Complement component C5 is crucial for experimental animal inflammatory tissue damage; however, its involvement in human inflammation is incompletely understood. The responses to gram-negative bacteria were here studied taking advantage of human genetic complement-deficiencies--nature's own knockouts--including a previously undescribed C5 defect. Such deficiencies provide a unique tool for investigating the biological role of proteins. The experimental conditions allowed cross-talk between the different inflammatory pathways using a whole blood model based on the anticoagulant lepirudin, which does not interfere with the complement system. Expression of tissue factor, cell adhesion molecules, and oxidative burst depended highly on C5, mediated through the activation product C5a, whereas gr

SUBMITTER: Lappegard KT 

PROVIDER: S-EPMC2732707 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature