The complement system, an enzyme cascade resembling the coagulation system, is built from almost 50 proteins, 10 different cell membrane proteins and is at work every day, in the healthy individual; in humans, 50% of C3 turns over within 24 hours.
Avacopan –> the orally administered C5aR inhibitor might reduce inflammatory damage in patients suffering from ANCA-associated vasculitis.
Genetic polymorphisms of C3 or of regulatory proteins can be predisposing for definite diseases, such as haemolytic uremic syndrome, HUS. If complement activation maintains health, its overreaction/persistent activation by autoantigen-antibody complexes leads to inflammatory reaction in those organs that contain much of the reticuloendothelial system (lung, liver, spleen, bone marrow) or where the microvasculature is quite strongly developed (kidney, skin). C5a may prime retinal pigment epithelial cells for inflammasome activation. Crosstalk C –> growth factor receptors, inflammasomes, metabolic sensors and the Notch system is seen.
C1q, tulip-like protein, subcomponent with C1r & C1s of the classical pathway plays a role in immunosenescence: C1q-Wnt/ß-catenin signals can be inhibited when angiotensin II receptor gets blocked, such as by prescribing irbesartran (Trade Name: Aprovel) (DOI: 10.1038/srep14453). Furthermore, C3/C1q made it into a list of frailty biomarkers along with insulin-like growth factor and adiponectin https://www.doi.org/10.1016/j.arr.2018.07.004
Morning_Evening (dawn_dim): C4,C3,CH50 the same dusk_dawn_C4C3CH50