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M.T. Lee, L.C. Hooper, L. Kump, R.N. Nussenblatt, J.J. Hooks, B. Detrick; Detection of Type 1 Interferons in Sera From Patients With Retinal Vasculitis . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5106.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Retinal vasculitis (RV), a major component of ocular inflammation, plays a critical role in retinal damage and subsequent vision loss. We have evaluated potential biological markers of RV and have recently identified elevated levels of the adhesion molecules, sE–selectin and sICAM–1. In this report we evaluated the interferons (IFN). Methods: Sera from a total of 36 RV patients were evaluated. They included 24 sera from 18 patients with Behcet’s Disease and 23 sera from 18 patients with idiopathic uveitis. Sera were also collected from 17 normal healthy individuals. All sera were EIA tested in duplicate for the presence of Interferon–alpha (IFN–α), Interferon–beta (IFN–ß) and Interferon gamma (IFN–γ). Human retinal microvascular endothelial cells were propagated in vitro. Following incubation with media or poly I:C, the supernatant fluids were evaluated by EIA for the presence of adhesion molecules or IFNs. Results: IFN–α, ß and γ were not detected in the sera from normal individuals and IFN–γ was not found in sera from RV patients. However, IFN– α and ß were detected in the sera from patients with RV. IFN–α was detected in 24% of the sera samples from Behcet’s patients (mean: 57 pg/ml, range: 16 – 161 pg/ml) and in 14% of the sera samples from uveitis patients (mean: 20 pg/ml, range: 17 – 23 pg/ml). IFN–ß was detected in 46% of the sera samples from Behcet’s patients (mean: 21 IU/ml, range: 1 – 91 IU/ml) and in 44% of the sera samples from uveitis patients (mean: 33 IU/ml, range: 6 – 69 IU/ml). Since the vascular endothelium is compromised in these patients, we evaluated human retinal microvascular endothelial cells in vitro as a possible source of the adhesion molecules, sE–selectin and sICAM–1, and the cytokines, IFN–α and ß. Treatment of cells with poly I:C for 4 or 24 hours induced the release of sE–selectin, sICAM–1 and IFN–ß. IFN–α was not detected. Conclusions: These data demonstrate that IFN–ß, sICAM–1 and E–selectin are detected in the sera of patients with retinal vaculitis and are produced by stimulated human retinal microvascular endothelial cells. IFN–ß, a mediator of innate immunity, is known to stabilize endothelial cell permeability and tight junction integrity and modify immune reactivity. It is possible that continued analysis of these biological markers may be useful in determining disease progression and identifying mechanisms of tissue damage
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