Complement system 1 6 4 5 1 3 5 7 8 Fig. 1 MBL MAC black blocks white boxes gray boxes  1 1 9 10 11 12 13 14 15 16 17 18 23 1 24 25 26 6 27 30 1 31 Role of complement in the protection of the normal eye 31 2 32 37 32 32 38 33 33 32 34 35 27 32 32 27 36 Role of complement in corneal disease 39 46 32 39 46 45 46 45 46 Pseudomonas aeruginosa 47 48 49 The aforementioned observations have important clinical implications. If in future anti-complement agents were to be considered for the treatment of corneal pathology, anaphylatoxins would be an ideal target for the patient presenting with chemical injury such as exposure to acid or alkali. On the other hand, in the case of bacterial infection both anti-anaphylatoxin and anti-MAC therapy should be considered. Although as discussed below the cornea possesses the ability to express different CRegs to protect itself from complement-mediated damage, it may not be able to upregulate various CRegs to an appropriate level during an acute episode of complement activation as observed during chemical insults or acute bacterial infection. In such cases, topical application of recombinant CRegs could be beneficial and serve as a better alternative for intervention. 2 2 27 33 50 33 2 51 Fig. 2 a b Epi S Endo AC  Role of complement in autoimmune uveitis 52 52 53 56 54 57 58 32 58 66 53 62 63 53 3 3 62 32 32 39 41 59 61 Fig. 3 I CB a d AC b e I CB AC c f  63 63 64 65 66 67 68 68 Thus, these studies provide strong evidence that the complement system and CRegs play an important role in the pathogenesis of autoimmune uveitis and provide alternative approaches for the development of effective therapy. More research in the future will present us enough information to develop anti-complement therapy for uveitis. Hopefully, in the future, complement inhibitors might be used as novel anti-uveitic agents in the clinic for the treatment of this important form of human ocular disease. Role of complement in age-related macular degeneration 69 71 69 71 72 71 72 73 75 73 75 76 79 76 79 80 81 82 cfh−/− 83 84 85 86 87 88 89 90 92 90 96 93 86 94 95 4 97 Fig. 4 CNV  50 93 94 98 99 In view of important developments relative to the role of the complement system in AMD during the past several years, we believe that the next decade would be critical for such studies. We hope that the interest will continue to grow in the future so that an alternative therapy could be developed by inhibiting complement activation. Since untreated CNV leads to the irreversible loss of central vision, it is important for the pharmaceutical companies to utilize the knowledge available to them from different research laboratories and should make every effort to transfer this knowledge to develop new drugs and therapies for AMD patients. Conclusions and clinical implications During the last decade, a lot of progress has been made to understand the pathophysiology of corneal diseases, uveitis, and macular degeneration. Specifically, the studies defining the role of the complement system in ocular diseases have drawn a lot of attention. It is an exciting area for future investigations and the basic questions such as what triggers the complement activation and which specific pathway is involved in corneal diseases, uveitis and macular degeneration need to be addressed. This understanding will help us to develop better therapies for ocular diseases in the future so that blindness could be prevented. The evidence derived from the studies reviewed here supports the concept that recombinant complement regulatory proteins may be therapeutically useful in the prevention of ocular tissue damage and in the treatment of various ocular diseases. Agents that specifically inhibit the complement system or complement activation products have been proven beneficial in the treatment of both human and experimental diseases over the past few years. Thus, the therapy based on complement inhibition has great potential in the future for the treatment of various ocular diseases such as keratitis, uveitis, and macular degeneration.