02000nas a2200313 4500000000100000008004100001260000900042653001800051653001500069653001000084653000900094653001700103653001800120653001100138653001600149653001100165653001200176653000900188653001600197653001800213653001200231100001500243700001300258245005600271300001000327490001600337520131900353022001401672 1985 d c198510aAcute disease10aAdolescent10aAdult10aAged10aCiliary Body10aCorneal Ulcer10aFemale10aHomeostasis10aHumans10aleprosy10aMale10aMiddle Aged10aT-Lymphocytes10aUveitis1 aMurray P I1 aRahi A H00aNew concepts in the control of ocular inflammation. a152-80 v104 ( Pt 2)3 a

Recent advances in the field of cellular immunology have enabled us to recognise a complex homeostatic mechanism controlling inflammation, allowing us to understand the aetiopathogenesis of many systemic disease processes. This immune regulatory mechanism involves the interaction of positive and negative messages passing between the different subsets of peripheral blood lymphocytes. Quantitative or qualitative defects in the suppressor cell subset of thymus derived T-lymphocytes are believed to be responsible (at least in part) for chronic inflammation and autoimmune disease. A variety of peripheral blood lymphocyte parameters were examined in four ill-understood inflammatory ophthalmological conditions: acute anterior uveitis, heterochromic cyclitis, acute lepromatous uveitis and Mooren's ulcer. Defects in the number or function of suppressor T-cells were found in all conditions studied. These findings make it possible to explain some of the immunological aberrations previously reported in these conditions. As abnormalities have been found in the immune regulatory mechanism of patients with inflammatory eye conditions of unknown aetiology, the way is now open to explore new lines of treatment using drugs which have the properties to allow selective manipulation of T-lymphocyte subsets.

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