CD11b and CD200 on Circulating Monocytes Differentiate Two Angiographic Subtypes of Polypoidal Choroidal Vasculopathy

We found that PCV is immunologically heterogeneous with significant differences between angiographic subtypes. Increased CD11b+ and CD200+ monocytes in those with a strong presence of BVN indicate that BVN development may be associated with retinal injury and a VEGF-mediated process that is either reflected or propelled by systemic changes in monocytes.

This was a prospective case-control study of patients with PCV (n = 27), age-matched healthy controls (n = 27), and patients with neovascular AMD (n = 49). All participants underwent a comprehensive ocular examination. Fluorescein and indocyanine green angiography were performed in patients suspected of neovascular AMD or PCV. Polypoidal choroidal vasculopathy was angiographically categorized into those with a strong presence of a branching vascular network (BVN) (type 1) or with a faint/no clear presence of a BVN (type 2). Fresh venous blood was stained with fluorescent antibodies for flow cytometric analyses. We compared the percentages of CD11b+, CD200+, and CD11b+CD200+ monocytes between groups of diagnosis and between different angiographic subtypes of PCV.

To investigate surface expression of CD11b and CD200 on circulating monocytes in patients with polypoidal choroidal vasculopathy (PCV).

Overall, CD11b+ monocytes were both increased in patients with PCV and neovascular AMD. CD200+ and CD11b+CD200+ monocytes were increased in patients with neovascular AMD. An age-related increase in CD11b+CD200+ monocytes was absent in patients with PCV and neovascular AMD. Patients with PCV type 1 had significantly higher CD11b+, CD200+, and CD11b+CD200+ monocytes, whereas patients with PCV type 2 had levels similar to that in healthy controls. Conclusions: We found that PCV is immunologically heterogeneous with significant differences between angiographic subtypes. Increased CD11b+ and CD200+ monocytes in those with a strong presence of BVN indicate that BVN development may be associated with retinal injury and a VEGF-mediated process that is either reflected or propelled by systemic changes in monocytes.