Complement C3 Affects Rac1 Activity in the Developing Brain
The complement system, which is part of the innate immune response system, has been recently shown to participate in multiple key processes in the developing brain.
Complement acts as a rapid and efficient immune surveillance system that has distinct effects on healthy and altered host cells and foreign intruders (reviews Walport, 2001a,b; Zipfel et al., 2007; Ricklin et al., 2010; Hawksworth et al., 2017). The complement system is composed of a large family of proteins, which are either secreted or membrane bound. These proteins are usually inactive until the system is triggered by stimuli. Complement is activated by three major routes: the classical, the alternative and the lectin pathways, all of which converge on complement component C3, a central molecule in the system that ultimately drives complement effector functions, including the elimination of pathogens, debris and cellular structures. Several complement proteins are cleaved during activation of the system; for example, C3 is cleaved into two fragments, C3a and C3b.
Collectively, our findings implicate Rac1 as one of the important downstream mediators of complement activity within the developing brain of the mouse embryo.
Common Design 