Figure 8
A predicted sequential model for the development of BPH-like tissue lesions through complement system activation in rat. Intracellular components of prostatic stromal cells, such as annexin, Hsp90, α-SMA, and β-actin, are exposed to the exterior of the cells likely due to infection, ischemia, or some other extracellular stimuli. Autoantibodies against the externalized components are developed under certain conditions, although the development mechanism is unclear, and antigen-antibody complexes are formed with the exposed intracellular autoantigens. The classical complement pathway is activated by binding of C1q to the complexes. Subsequently, activation of the lectin and alternative pathways occurs to accelerate the cleavage of C3 and C5, leading to the formation of anaphylatoxins (C3a and C5a) and the terminal pathway complex C5b-9. Our results strongly suggest that the complement system plays a role in the development of BPH-like tissue lesions in the rat BPH model via this mechanism.
