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Updated: May 22, 2026
Characterization of Vascular Morphology of Neovascular Age-Related Macular Degeneration by Indocyanine Green Angiography
Published on: August 11, 2023
Altered expression of CD46 and CD59 on leukocytes in neovascular age-related macular degeneration
Amardeep Singh1, Carsten Faber, Mads Falk
1Department of Ophthalmology, Copenhagen University Hospital, Roskilde, Denmark. asingh@dadlnet.dk
Insights
Neovascular age-related macular degeneration (AMD) shows lower expression of complement proteins CD46 and CD59 on monocytes. This suggests inadequate complement system regulation in AMD pathogenesis.
Area of Science:
- Ophthalmology
- Immunology
- Genetics
Background:
- Age-related macular degeneration (AMD) is a leading cause of vision loss.
- The complement system plays a role in inflammatory processes.
- Complement regulatory proteins (CRPs) like CD46, CD55, and CD59 modulate complement activity.
Purpose of the Study:
- To investigate the expression of CD46, CD55, and CD59 on peripheral leukocytes in neovascular AMD.
- To determine if complement dysregulation is associated with neovascular AMD.
Main Methods:
- Prospective case-control study.
- Involved 35 patients with neovascular AMD and 30 controls.
- Flow cytometry was used to quantify CRP expression on monocytes, lymphocytes, and granulocytes.
Main Results:
- Significantly lower expression of CD46 and CD59 on monocytes in neovascular AMD patients versus controls.
- Lower CD46 expression on lymphocytes in patients with fibrosis compared to those without fibrosis.
Conclusions:
- Neovascular AMD is linked to impaired complement system regulation.
- Findings support the role of complement dysregulation in AMD pathogenesis.
Purpose:
To investigate the expression of the complement regulatory proteins CD46, CD55, and CD59 on peripheral leukocytes in neovascular age-related macular degeneration (AMD).
Design:
Prospective, case-control study.
Methods:
Thirty-five unrelated patients with neovascular AMD and 30 control individuals were included in this case-control study. All participants were subjected to a structured interview and detailed imaging (autofluorescence, digital funduscopy, spectral-domain optical coherence tomography, and fluorescein and indocyanine green angiography in patients suspected of having neovascular AMD) was performed. Fresh ethylenediamine-tetraacetic acid blood was obtained and stained with monoclonal antibodies. Using flow cytometry, the percentage of CD14(+) monocytes, CD45(+) lymphocytes, and CD45(+) granulocytes positive for CD46, CD55, and CD59 was determined in patients with neovascular AMD and was compared with that of controls.
Results:
We found that the expression of CD46 and CD59 was significantly lower on CD14(+) monocytes in patients with neovascular AMD compared with controls (P = .0070). A significantly lower expression of CD46 on lymphocytes was observed in patients with fibrosis compared with patients without fibrosis (P = .010).
Conclusions:
Our study suggests that neovascular AMD is associated with an inadequate regulation of the complement system, supporting current evidence on the role of complement dysregulation in the pathogenesis of AMD.
