M. W. Johnson, “Etiology and treatment of macular edema,” American Journal of Ophthalmology, vol. 147, no. 1, pp. 11–21, 2009.
[2]
E. Buschini, A. Piras, R. Nuzzi, and A. Vercelli, “Age related macular degeneration and drusen: neuroinflammation in the retina,” Progress in Neurobiology, vol. 95, no. 1, pp. 14–25, 2011.
[3]
A. M. Joussen, V. Poulaki, M. L. Le et al., “A central role for inflammation in the pathogenesis of diabetic retinopathy,” FASEB Journal, vol. 18, no. 12, pp. 1450–1452, 2004.
[4]
J. P. Ehlers and S. Fekrat, “Retinal vein occlusion: beyond the acute event,” Survey of Ophthalmology, vol. 56, no. 4, pp. 281–299, 2011.
[5]
N. Yoshida, Y. Ikeda, S. Notomi, et al., “Clinical evidence of sustained chronic inflammatory reaction in retinitis pigmentosa,” Ophthalmology, vol. 120, no. 1, pp. 100–105, 2013.
[6]
S. Sugita, “Role of ocular pigment epithelial cells in immune privilege,” Archivum Immunologiae et Therapiae Experimentalis, vol. 57, no. 4, pp. 263–268, 2009.
[7]
T. C. Nag and S. Wadhwa, “Ultrastructure of the human retina in aging and various pathological states,” Micron, vol. 43, no. 7, pp. 759–781, 2012.
[8]
H. Xu, M. Chen, and J. V. Forrester, “Para-inflammation in the aging retina,” Progress in Retinal and Eye Research, vol. 28, no. 5, pp. 348–368, 2009.
[9]
G. S. Hageman, P. J. Luthert, N. H. V. Chong, L. V. Johnson, D. H. Anderson, and R. F. Mullins, “An integrated hypothesis that considers drusen as biomarkers of immune-mediated processes at the RPE-Bruch's membrane interface in aging and age-related macular degeneration,” Progress in Retinal and Eye Research, vol. 20, no. 6, pp. 705–732, 2001.
[10]
G. S. Hageman, D. H. Anderson, L. V. Johnson et al., “A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration,” Proceedings of the National Academy of Sciences of the United States of America, vol. 102, no. 20, pp. 7227–7232, 2005.
[11]
A. O. Edwards, R. Ritter III, K. J. Abel, A. Manning, C. Panhuysen, and L. A. Farrer, “Complement factor H polymorphism and age-related macular degeneration,” Science, vol. 308, no. 5720, pp. 421–424, 2005.
[12]
J. L. Haines, M. A. Hauser, S. Schmidt et al., “Complement factor H variant increases the risk of age-related macular degeneration,” Science, vol. 308, no. 5720, pp. 419–421, 2005.
[13]
R. J. Klein, C. Zeiss, E. Y. Chew et al., “Complement factor H polymorphism in age-related macular degeneration,” Science, vol. 308, no. 5720, pp. 385–389, 2005.
[14]
J. E. Shaw, R. A. Sicree, and P. Z. Zimmet, “Global estimates of the prevalence of diabetes for 2010 and 2030,” Diabetes Research and Clinical Practice, vol. 87, no. 1, pp. 4–14, 2010.
[15]
J. Tang and T. S. Kern, “Inflammation in diabetic retinopathy,” Progress in Retinal and Eye Research, vol. 30, no. 5, pp. 343–358, 2011.
[16]
A. M. Joussen, T. Murata, A. Tsujikawa, B. Kirchhof, S.-E. Bursell, and A. P. Adamis, “Leukocyte-mediated endothelial cell injury and death in the diabetic retina,” American Journal of Pathology, vol. 158, no. 1, pp. 147–152, 2001.
[17]
A. G. Harris, T. C. Skalak, and D. L. Hatchell, “Leukocyte-capillary plugging and network resistance are increased in skeletal muscle of rats with streptozotocin-induced hyperglycemia,” International Journal of Microcirculation, vol. 14, no. 3, pp. 159–166, 1994.
[18]
N. Bhagat, R. A. Grigorian, A. Tutela, and M. A. Zarbin, “Diabetic macular edema: pathogenesis and treatment,” Survey of Ophthalmology, vol. 54, no. 1, pp. 1–32, 2009.
[19]
W. J. Lee, M. H. Kang, M. Seong, and H. Y. Cho, “Comparison of aqueous concentrations of angiogenic and inflammatory cytokines in diabetic macular oedema and macular oedema due to branch retinal vein occlusion,” British Journal of Ophthalmology, vol. 96, no. 11, pp. 1426–1430, 2012.
[20]
M. J. Koss, M. Pfister, F. Rothweiler et al., “Comparison of cytokine levels from undiluted vitreous of untreated patients with retinal vein occlusion,” Acta Ophthalmologica, vol. 90, no. 2, pp. e98–e103, 2012.
[21]
H. Noma, H. Funatsu, M. Yamasaki et al., “Pathogenesis of macular edema with branch retinal vein occlusion and intraocular levels of vascular endothelial growth factor and interleukin-6,” American Journal of Ophthalmology, vol. 140, no. 2, pp. 256–261, 2005.
[22]
H. Noma, H. Funatsu, M. Yamasaki et al., “Aqueous humour levels of cytokines are correlated to vitreous levels and severity of macular oedema in branch retinal vein occlusion,” Eye, vol. 22, no. 1, pp. 42–48, 2008.
[23]
D. A. Newsome and R. G. Michels, “Detection of lymphocytes in the vitreous gel of patients with retinitis pigmentosa,” American Journal of Ophthalmology, vol. 105, no. 6, pp. 596–602, 1988.
[24]
C. J. J. Brinkman, A. J. L. G. Pinckers, and R. M. Broekhuyse, “Immune reactivity to different retinal antigens in patients suffering from retinitis pigmentosa,” Investigative Ophthalmology and Visual Science, vol. 19, no. 7, pp. 743–750, 1980.
[25]
J. H. Yamamoto, O. Okajima, M. Mochizuki et al., “Cellular immune responses to retinal antigens in retinitis pigmentosa,” Graefe's Archive for Clinical and Experimental Ophthalmology, vol. 230, no. 2, pp. 119–123, 1992.
[26]
S. A. Tamm, S. M. Whitcup, I. Gery, B. Wiggert, R. B. Nussenblatt, and M. I. Kaiser-Kupfer, “Immune response to retinal antigens in patients with gyrate atrophy and other hereditary retinal dystrophies,” Ocular Immunology and Inflammation, vol. 9, no. 2, pp. 75–84, 2001.