Figure 1
Complement activation is initiated through three pathways: the
classical, alternative or the lectin pathway. Full activation leads to
the generation of several biologically active fragments including C5b-9,
which ‘seeds’ membrane attack complex (MAC)-mediated direct lysis of
pathogens. In addition, complement and extra- as well as intracellular
complement receptors also fine shape cells of the innate and the
adaptive immune system. Polymorphic neutrophils (PMN) and
monocyte/macrophages express anaphylatoxin receptors. Dendritic cells
can be identified by expression CD11c, a component of complement
receptor 4. Dendritic cells also express the CD11b, a component of
complement receptor 3. T cells express anaphylatoxin receptors in
different intracellular compartments and on the surface. Intracellular
C3 is converted by cathpepsin L to C3a that bind lysosomal C3aR. This
drives mammalian target of rapamycin (mTOR) activity that sustains
homeostatic cell survival. C5aR1 is found on the surface was well as on
mitochondria whereas C5aR2 is only found on the surface. B cells express
complement receptors 1 and 2 (CR1/CR2). Complement proteins, innate and
adaptive immune cells are potential mediators of hypertension and
hypertensive end organ damage. Endothelial dysfunction and injury are
most likely the first step of hypertensive end organ injury.