Purpose <p>Age-related macular degeneration (AMD) is a multifactorial disease that leads to progressive central vision loss. Bevacizumab (Avastin), a therapeutic agent used in the treatment of AMD, exerts its effect by binding to all isoforms of vascular endothelial growth factor (VEGF), thereby inhibiting angiogenesis. This study aimed to investigate the effects of Bevacizumab on immune system cells in the context of neovascular AMD (nAMD) treatment.</p> Methods <p>Patients with nAMD receiving Bevacizumab treatment (<i>n</i> = 18) and a control group of individuals undergoing cataract surgery (<i>n</i> = 19) were included in the study. Peripheral blood samples were collected from nAMD patients before Bevacizumab treatment (baseline, 0 month) and after three monthly intravitreal injections. Following staining with monoclonal antibodies, innate immune cell, T cell, and B cell subsets were analyzed using flow cytometry panels.</p> Results <p>In the innate immune cell subsets of patients with neovascular AMD (nAMD), immature and suppressive neutrophils were significantly increased, whereas intermediate and non-classical monocytes were significantly decreased. Following intravitreal bevacizumab (IVB) treatment, these cell populations tended to return toward baseline levels. In the adaptive immune compartment, effector memory (EM) T cell subsets, particularly EM1 (effector memory 1) and EM3 (effector memory 3), exhibited opposing dynamics, showing significant changes both before and after IVB treatment.</p> Conclusion <p>In conclusion, the findings from this study provide preliminary evidence that various immune cell subsets in both innate and adaptive compartments show associations with AMD pathogenesis and with IVB treatment.</p>