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Interleukin-1 and tumor necrosis factor-alpha: novel targets for immunotherapy in Eales disease.

Authors: Saxena, S  Pant, AB  Khanna, VK  Agarwal, AK  Singh, K  Kumar, D  Singh, VK 
Citation: Saxena S, etal., Ocul Immunol Inflamm. 2009 May-Jun;17(3):201-6. doi: 10.1080/09273940902731015.
Pubmed: (View Article at PubMed) PMID:19585364
DOI: Full-text: DOI:10.1080/09273940902731015

BACKGROUND: Eales disease is an idiopathic obliterative vasculopathy that primarily affects the peripheral retina of young adults. The authors evaluated interleukin 1 beta (IL-1beta), interleukin-6 (IL-6), Interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-alpha) in the serum of patients with Eales disease stages for the first time. METHODS: The study group consisted of 45 consecutive patients of Eales disease [inflammatory stage (n = 15) and proliferative stage (n = 30)] and 28 healthy controls. Immunoassays for the quantification of the levels of four cytokines including IL-1beta, IL-6, IL-10, and TNF-alpha in the serum samples were performed using ELISA kits. RESULTS: IL-1beta, IL-6, IL-10, and TNF-alpha levels were found to be increased significantly in the inflammatory stage of Eales disease as compared to controls (p < .001). IL-1beta levels decreased significantly during the proliferative stage of the disease as compared to the inflammatory stage (p = .03). TNF-alpha levels increased significantly during the proliferative stage as compared to the inflammatory stage (p = .02). CONCLUSIONS: Raised levels of IL-1beta and TNF-alpha were observed in the inflammatory stage and persisted in the proliferative stage of the disease. The IL-1 system and TNF-alpha represent novel target for immunotherapy for controlling inflammatory activity and/or the associated long-term sequelae related to angiogenesis in Eales disease.


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CRRD Object Information
CRRD ID: 7401211
Created: 2013-11-07
Species: All species
Last Modified: 2013-11-07
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.