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Baoying Liu, H Nida Sen, Diamond Ling, megan casady, Shayma Jawad, Zhiyu Li, Lai Wei, Robert B. Nussenblatt; Glucocorticoid Increases Cd14HighCd16+ Monocyte Population And Contributes To Uveitis Therapy. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5497.
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Corticosteroid is the mainstay of uveitis treatment. Monocytes and macrophages have been reported to contribute to uveitis pathogenesis. The goal of this study is to investigate the influence of glucocorticoids (dexamethasone) on human monocytes and its implications for uveitis therapy.
Human peripheral blood mononuclear cells (PBMCs) were isolated from the blood of healthy donors using a Ficoll gradient centrifugation protocol. Monocyte phenotyping was performed based on a 4-color flow cytometry staining protocol. Apoptotic cells were stained with the combination of annexin-V-FITC and Via-probeTM (7-Amino-actinomycin D, 7-AAD) and detected by flow cytometry.
Dexamethasone increased CD14highCD16+ monocyte population in vitro. This effect was not due to dexamethasone induced cell death of CD14highCD16- monocytes. Rather, dexamethasone protected both CD14highCD16+ and CD14highCD16- monocytes from undergoing apoptosis to a similar extent. Dexamethasone converted CD14highCD16- monocytes to CD14highCD16+ in cell culture. Consistent with in vitro results, we observed a higher percentage of CD14highCD16+ monocyte population in prednisone treated uveitis patients.
The conversion of monocytes from CD14highCD16- to CD14highCD16+ by dexamethasone suggests an immune regulatory role of CD14highCD16+ monocytes. Understanding the influence of glucocorticoids on human monocytes may be useful in understanding the mechanisms of monocytes in the pathogenesis and treatment of uveitis.
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