Abstract
Polypoidal choroidal vasculopathy (PCV) and neovascular age-related macular degeneration (AMD) are prevalent age-related diseases characterized by exudative changes in the macula. Although they share anatomical and clinical similarities, they are also distinctly characterized by their own features, e.g. vascular abnormalities in PCV and drusen-mediated progression in neovascular AMD. PCV remains etiologically uncharacterized, and ongoing discussion is whether PCV and neovascular AMD share the same etiology or constitute two substantially different diseases. In this study, we investigated T-cell differentiation and aging profile in human patients with PCV, patients with neovascular AMD, and age-matched healthy control individuals. Fresh venous blood was prepared for flow cytometry to investigate CD4+ and CD8+ T-cell differentiation (naïve, central memory, effector memory, effector memory CD45ra+), loss of differentiation markers CD27 and CD28, and expression of aging marker CD56. Patients with PCV were similar to the healthy controls in all aspects. In patients with neovascular AMD we found significantly accelerated T-cell differentiation (more CD28−CD27− cells) and aging (more CD56+ cells) in the CD8+ T-cell compartment. These findings suggest that PCV and neovascular AMD are etiologically different in terms of T cell immunity, and that neovascular AMD is associated with T-cell immunosenescence.
Highlights
Aging is the greatest risk factor of developing agerelated macular degeneration (AMD) — the most common reason of irreversible vision loss and blindness in the elderly [1,2]
These findings suggest that Polypoidal choroidal vasculopathy (PCV) and neovascular age‐related macular degeneration (AMD) are etiologically different in terms of T cell immunity, and that neovascular AMD is associated with T‐cell immunosenescence
Are PCV and neovascular AMD etiologically similar or different? In this study, we looked at this question in terms of systemic T-cell profile of differentiation and aging
Summary
Aging is the greatest risk factor of developing agerelated macular degeneration (AMD) — the most common reason of irreversible vision loss and blindness in the elderly [1,2]. Zeng et al investigated extracellular tissue homeostasis and found increased level of serum matrix metalloproteinases 2 and 9 in patients with PCV compared to patients with neovascular AMD and healthy controls [20] Genetic studies suggest both similarities and differences and at present generally neither confirm nor reject a possible association of PCV with alterations in the immune system [21]. Our aim with this study was to investigate T-cell aging and differentiation by mapping the differentiation profile and investigating the proportion of CD56+ Tcells in different differentiation subsets in patients with PCV and compare the results to that of patients with neovascular AMD and healthy controls
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