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

机译:测量血清和玻璃体浓度的抗型II胶原蛋白抗体在β患者视网膜病变

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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.
机译:背景:自身免疫机制已被假定为糖尿病视网膜病变(DR)的原因,因为据报道,在博士患者的血清中检测到几种自身抗体。在本研究中,我们测量了患者博士中的血清和玻璃体水平的抗型II胶原(抗-II-C)抗体,并研究了它们与Dr.Patients和方法的发育机制的关联:从患者获得血液样品患有增殖性博士和患有糖尿病Marumare水肿的患者,在大阪医学院,大阪市,大阪市,大阪市,大阪市玻璃体切除术。没有DR的糖尿病患者也包括在内。该对照组由年龄和性别匹配的患者组成,患者患有用于视网膜脱离或白内障的眼科手术的无炎症眼病。使用人/猴抗-II-C IgG测定试剂盒测量玻璃体和血清中的抗-II-C免疫球蛋白(Ig)G抗体的水平。结果:抗-II-C IgG抗体的血清水平显着博士患者高于患有非炎症眼病的患者(56.8±33.8单位/ ml,分别为30.5±13.7单位/ ml; P <0.05,Fisher的确切测试)。糖尿病患者在没有博士的患者中也显着高于非炎症眼病患者(76.3±49.7单位/ ml,分别为30.5±13.7个单位/ ml; P <0.01,Fisher的确切测试)。然而,在所有得到的玻璃体流体样品中不能检测到抗-II-C IgG抗体水平。结论:DR的显影和进展可能与涉及眼内II型胶原蛋白的机制有关,这通常具有免疫耐受性螯合螯合剂。在DR中,血管屏障的破坏导致人眼内II型胶原和免疫竞争细胞之间接触,并随后激活自身免疫机制。

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