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Measurement of serum and vitreous concentrations of anti-type II collagen antibody in diabetic retinopathy

Authors Nakaizumi A, Fukumoto M, Kida T, Suzuki H, Morishita S, Satou T, Oku H, Ikeda T, Nakamura K

Received 6 October 2014

Accepted for publication 2 December 2014

Published 20 March 2015 Volume 2015:9 Pages 543—547

DOI https://doi.org/10.2147/OPTH.S75422

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Scott Fraser


Atsuko Nakaizumi,1 Masanori Fukumoto,1 Teruyo Kida,1 Hiroyuki Suzuki,1 Seita Morishita,1 Takaki Satou,1 Hidehiro Oku,1 Tsunehiko Ikeda,1 Kimitoshi Nakamura2

1Department of Ophthalmology, Osaka Medical College, Takatsuki City, Osaka, 2Nakamura Eye Clinic, Nagano, Japan


Background: Autoimmune mechanisms have been postulated as a cause of diabetic retinopathy (DR), as several autoantibodies have reportedly been detected in the serum of DR patients. In this present study, we measured serum and vitreous levels of anti-type II collagen (anti-II-C) antibodies in DR patients and investigated their association with the mechanism of development of DR.
Patients and methods: Blood samples were obtained from patients with proliferative DR and from patients with diabetic macular edema who underwent vitrectomy at Osaka Medical College, Takatsuki City, Osaka, Japan. Diabetic patients without DR were also included. The control group consisted of age- and sex-matched patients with noninflammatory eye diseases who underwent eye surgery for retinal detachment or for cataracts. The levels of anti-II-C immunoglobulin (Ig)G antibody in the vitreous and serum were measured using a human/monkey anti-II-C IgG assay kit.
Results: The serum levels of anti-II-C IgG antibody were significantly higher in the DR patients than in the patients with noninflammatory eye disease (56.8±33.8 units/mL versus 30.5±13.7 units/mL, respectively; P<0.05, Fisher’s exact test). These levels were also significantly higher in the diabetic patients without DR than in the patients with noninflammatory eye disease (76.3±49.7 units/mL versus 30.5±13.7 units/mL, respectively; P<0.01, Fisher’s exact test). However, anti-II-C IgG antibody levels were unable to be detected in all of the obtained vitreous fluid samples.
Conclusion: The development and progression of DR may be related to a mechanism involving intraocular type II collagen, which normally has immunological tolerance as a sequestered antigen. In DR, the disruption of the blood–retinal barrier leads to contact between the intraocular type II collagen and immunocompetent cells, and to subsequent activation of the autoimmune mechanism.

Keywords: blood–retinal barrier, autoimmune mechanism, vitreous, serum

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