On a cellular level, it has been shown that C5a effectively interacts with cells and modulates their apoptosis rate. Interestingly, the effects on programmed cell death seem to be cell dependent, with a higher rate of apoptosis in thymocytes (37,40) but decreased apoptosis in neutrophils (39, 63, 64) . Overall, the C5ainduced changes point toward an enhanced susceptibility toward infections, as well as to a prolonged presence of neutrophils resulting in an exaggerated inflammatory response and host damage. 