2006;39:41C54. three antigens. Asymptomatic anti-serum-positive individuals showed a higher frequency of anti-human whole retina extract antibodies in comparison to asymptomatic anti-serum-negative patients. The bovine S-antigen and interphotoreceptor retinoid-binding protein ELISAs also showed a higher mean reactivity in the uveitis groups compared to the asymptomatic group, but the observed reactivities were lower and overlapped without discrimination. CONCLUSION: We detected higher levels of anti-retina antibodies in uveitis patients and in a small fraction of asymptomatic patients with chronic toxoplasmosis. The presence of anti-retina antibodies in sera might be a marker of eye disease in asymptomatic patients, especially when whole human retina extract is used in a solid-phase ELISA. Keywords: Retina, Uveitis, Toxoplasmosis, Autoantibodies, ELISA INTRODUCTION Individuals with uveitis may present with visual loss depending on the location of the site of inflammation.1 The most prominent feature of uveitis is the inflammatory process, which is characterized by an intraocular immune response with several infectious and non-infectious etiologies.2 Most H3B-6527 of the physiopathological studies of uveitis have focused on the antigens that trigger the inflammatory process, which can be an autoimmune response to retina proteins3 or an infectious agent.1 Two bilateral granulomatous uveitis conditions, sympathetic ophthalmia (SO) and Vogt-Koyanagi-Harada (VKH) disease, share several clinical, histological and immunohistochemical features despite exhibiting diverse triggering events.4 In these two uveitis conditions, HLA-DR4 and T-cell responses H3B-6527 are associated with retina antigens, which indicates the presence of an underlying T-cell-mediated autoimmunity to uveal/retinal antigens during their development.3,4 The only reported reliable feature that could differentiate SO from VHK disease is a history of a penetrating wound in SO and the absence of such trauma in VKH disease. The intraocular compartment lacks lymphatic drainage system and appears to function similarly to a number of alymphatic biological sites that present alterations in immune functions and antigen presentation.5 In an SO experimental model, a subconjunctival injection of retina S-antigen in one eye induced a bilateral sympathetic uveitis, whereas an intraocular injection in one eye did not induce disease.6 However, autoimmune antibodies against the outer segments of photoreceptors and Muller cells have been detected in patients with VKH disease, in some patients with Behcet’s syndrome, and in a few patients with sympathetic ophthalmia.7 These results suggest that retina autoimmunity may play an important role in H3B-6527 the pathogenesis of posterior H3B-6527 uveitis and that anti-retina antibodies are present in this condition. infection is usually asymptomatic in humans, and persistent infection with the cyst form of this parasite is controlled by the host immune system. However, in fetuses and immunosuppressed patients (such as AIDS patients or organ transplant recipients), the parasite becomes activated and causes life-threatening disease.9 A specific retina involvement may be present in up to 20% of all infected individuals, regardless of their immune status. 10 Toxoplasmosis is the most frequent Rabbit Polyclonal to HLX1 cause of posterior uveitis in the USA and Brazil, and it is associated with visual impairment and blindness. The diagnosis is usually based on characteristic fundoscopy findings and the clinical presentation; the disease is usually progressive and recurrent, and it can cause severe morbidity. These outcomes occur despite the availability of an effective treatment based on pyrimethamine, which is an anti-parasitic drug that is associated with anti-inflammatory drugs such as corticosteroids.11 In the eye, the primary target tissue for ocular toxoplasmosis is the neural retina, which displays a surrounding, intense granulomatous reaction with numerous intracellular parasite cysts.12 Free tachyzoites and cysts are also observed within retina pigment epithelium (RPE) cells.13 Ocular reactions also involve necrosis of the retina and RPE, subretinal and choroidal neovascularization, and focal inflammation.14 The inflammatory processes that are associated with retina infection by may damage Bruch’s membrane, which results in a disruption of the choroidoretinal interface.4 uveitis can present the same autoimmune response as SO and VKH: a disruption of the parasite cysts that exposes the retina antigens. When central eyesight can be threatened, ocular toxoplasmosis can be treated with particular antibiotics with corticosteroids collectively, which implies that the sponsor immune response takes on an active part.