Whittle R M, Wallace G R, Whiston R A, Dumonde D C, Stanford M R
Department of Immunology, Rayne Institute, St Thomas's Hospital, London.
Br J Ophthalmol. 1998 Sep;82(9):1017-21. doi: 10.1136/bjo.82.9.1017.
BACKGROUND/AIMS: Toxoplasma retinochoroiditis (TR) is an important cause of blindness and visual morbidity, affecting young adults. It has been postulated that some of the retinal damage observed in TR is due to antiretinal autoimmune mechanisms.
Humoral antiretinal autoimmunity in TR was investigated by indirect immunofluorescence (IIF) on normal human cadaveric retina and by a human retinal S-antigen ELISA. 36 patients with TR were separated on clinical grounds into those with first recurrence of disease (n = 18) or those with multiple recurrences (n = 18). Patients were also segregated into those with active (n = 28) or quiescent disease (n = 8). Serum from 16 normal controls (six with positive toxoplasma serology and 10 without) with no evidence of eye disease and 12 patients with idiopathic retinal vasculitis (IRV) were also tested.
Sera from 34 of the 36 patients (94%) with TR demonstrated photoreceptor layer reactivity by IIF contrasting with six of 16 normal controls (p = < 0.001) and three of 12 IRV patients (p = < 0.001). Titres of antiphotoreceptor antibody were also higher among TR patients than controls. Sera from 27 of the 36 TR patients, 10 of 16 normals, and nine of 12 retinal vasculitis patients possessed anti-human retinal S-antigen antibodies at a titre of 1:400 or more as assessed by ELISA (p = > 0.05). Antiretinal autoantibody as detected by IIF did not run in parallel with S-antigen reactivity.
The data indicate that the extent of antiretinal reactivity within TR is not accounted for by anti-S-antigen antibodies alone. This remarkably high prevalence of antiphotoreceptor antibody in TR as opposed to that found in either healthy or disease controls suggest that these antibodies may be co-pathogenic in toxoplasma retinochoroiditis.
背景/目的:弓形虫视网膜脉络膜炎(TR)是导致年轻人失明和视力损害的重要原因。据推测,TR中观察到的一些视网膜损伤是由抗视网膜自身免疫机制引起的。
通过对正常人尸体视网膜进行间接免疫荧光法(IIF)和人视网膜S抗原酶联免疫吸附测定(ELISA),研究TR中的体液抗视网膜自身免疫。36例TR患者根据临床情况分为疾病首次复发组(n = 18)和多次复发组(n = 18)。患者还被分为疾病活动组(n = 28)或静止组(n = 8)。对16名无眼部疾病证据的正常对照者(6名弓形虫血清学阳性,10名阴性)和12例特发性视网膜血管炎(IRV)患者的血清也进行了检测。
36例TR患者中有34例(94%)的血清通过IIF显示出光感受器层反应性,与之形成对比的是,16名正常对照者中有6例(p = < 0.001),12例IRV患者中有3例(p = < 0.001)。TR患者中抗光感受器抗体的滴度也高于对照组。通过ELISA评估,36例TR患者中有27例、16名正常对照者中有10例以及12例视网膜血管炎患者中有9例的血清具有滴度为1:400或更高的抗人视网膜S抗原抗体(p = > 0.05)。通过IIF检测到的抗视网膜自身抗体与S抗原反应性并不平行。
数据表明,TR中抗视网膜反应的程度并非仅由抗S抗原抗体引起。与健康对照者或疾病对照者相比,TR中抗光感受器抗体的高患病率表明,这些抗体可能在弓形虫视网膜脉络膜炎中具有共同致病性。