Anterior endogenous uveitis and HLA-B27 antigen

Zhaboedov, G.; Ivanova, N.; Kopaenko, A.

doi:10.31288/oftalmolzh201036166

Cited by 1 publication

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“…The capacity for ocular and lymph node immune tolerance is however not always adequate to inhibit autoreactive T cell proliferation. The inherited susceptibility to autoimmune processes, when combined with antigenic mimicry between bacterial/viral endotoxins and synovium/uveal tract proteins, results in impairment of immune tolerance and production of antibodies against selfantigens [3,8,26].…”

Section: Mechanisms Of Immunotolerance Toward Ocular Antigensmentioning

confidence: 99%

“…Each recurrence causes cell re-migration to the anterior chamber, and exudation of cytokines, growth factors, and fibrinogen to the anterior aqueous humor and tissues. All these things together result in alterations in aqueous humor dynamics, opacification of the optical media, and interstitial retinal edema, which significantly decreases the chances for complete visual recovery [8,16,23]. Nevertheless, under some circumstances, ophthalmologists miss some of the signs of inflammation during the routine examination of the anterior chamber.…”

Section: Clinical Characteristics Of Uveitismentioning

confidence: 99%

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Immune Mechanisms, Clinical Features and Course of Non-infectious Uveitis

Sydorova¹,

Kondratiuk²,

Бычкова³

2015

Oftalmol Zh

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In most countries, the uveitides are responsible for 5-13% of all cases of blindness. Non-infectious uveitides are divided into those with and without known systemic association (both in children and adults). The Standardization of Uveitis Nomenclature (SUN) Working Group used anatomic location of the inflammation as an ontologic dimension, defined the criteria for the activity of inflammatory process, divided uveitis into groups and subgroups based on its course, and defined the tactical treatment algorithm. The uveitis development is based mainly on the alterations in the mechanisms of immunotolerance toward self ocular antigens, and on the emergence of autoagression toward these antigens. An alteration in immune tolerance to ocular antigens occurs if (1) regulatory CD25 + T cell subset is insufficient, and (2) B cells are activated with production of specific antibodies to the uveal tract structures. Systemic therapeutical agents for uveitis include corticosteroids, nonsteroidal anti-inflammatory drugs, cytostatics and immunobiologic agents. There are, however, no clinical guidelines involving the uveitis treatment approaches listed. The analysis of correlations between the degree of the alterations in the immune system and the course of uveitis will allow the development of the algorithm for the treatment of uveal inflammation entities.

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Section: Mechanisms Of Immunotolerance Toward Ocular Antigensmentioning

confidence: 99%

Section: Clinical Characteristics Of Uveitismentioning

confidence: 99%