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. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: Immunotherapy. 2010 Jul;2(4):511–520. doi: 10.2217/imt.10.33

Figure 1. Multiple processes contribute to the development of chronic rejection.

Figure 1

Both alloantigen-dependent and -independent factors promote immune responses against allografts and activation of graft endothelium. Complex interplay of these factors results in graft infiltration/inflammation and injury. Injury prompts reparative processes characterized by fibroblast activation and recruitment, as well as proliferation and migration of smooth muscle-like cells in the vasculature. These processes lead to the development of chronic rejection hallmarks of chronic allograft vasculopathy and interstitial fibrosis. Graft hypertrophy, characterized by increased cardiomyocyte size and thickening of the left ventricle wall, accompanies these pathologies, although the interrelationship between these processes is not yet understood. Ultimately, these graft pathologies lead to organ dysfunction and failure.