RPE Bruch´s membrane Choriocapillaris
Recently it has been proposed that AMD could be a chronic inflammation and a local immune reaction much in analogy to other degenerative diseases correlated with age e.g. Alzheimer’s disease and atherosclerosis where a local chronic inflammation is elicited by cellular damage and the accumulation of insoluble amyloid deposits. Several inflammatory subsystems have been implicated e.g. the complement system, cytokines and chemokines, acute phase proteins, the coagulation/fibrinolysis system as well as the auto-immune system (Mullins, Russell et al.
2000; Hageman, Luthert et al. 2001). Common to many inflammatory diseases is the recruitment of macrophages and antigen presenting cells e.g. dendritic cells both systemically and locally (microglia) (Penfold, Madigan et al. 2001). Adhesion molecules on endothelial cells (EC) enhance accumulation and local binding of leukocytes in inflammation (Fig 4).
The leukocytes can stimulate CNV growth by VEGF release enhancing EC mitosis and capillary permeability as well as regulation of immunoresponse, inflammation and wound healing through production of interleukines and TNF-Į.
Fig 4. Main events leading to the invasion of a target organ by cells from the circulation
(Reprinted with kind permission from Montan, P (2000): Immunological and inflammatory mechanisms in ocular allergy with special reference to vernal keratoconjunctivitis. Clinical and experimental studies. Thesis, KI, Stockholm)