Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
Anti-IL-17RA enhances the efficacy of anti-VEGF
Author Affiliations & Notes
  • Brooklyn E. Taylor
    Ophthalmology, Case Western Reserve University School of Medicine, Cleveland, Ohio, United States
    Research, VA Northeast Ohio Healthcare System, Cleveland, Ohio, United States
  • Katherine Barber
    Research, VA Northeast Ohio Healthcare System, Cleveland, Ohio, United States
  • Chieh Lee
    Ophthalmology, Case Western Reserve University School of Medicine, Cleveland, Ohio, United States
  • Scott J Howell
    Research, VA Northeast Ohio Healthcare System, Cleveland, Ohio, United States
  • Patricia R Taylor
    Ophthalmology, Case Western Reserve University School of Medicine, Cleveland, Ohio, United States
    Research, VA Northeast Ohio Healthcare System, Cleveland, Ohio, United States
  • Footnotes
    Commercial Relationships   Brooklyn Taylor None; Katherine Barber None; Chieh Lee None; Scott Howell None; Patricia Taylor None
  • Footnotes
    Support  NIH R01 EY030487, NIH U01 EY034693, VA Merit CX002204, NIH P30 EY011373
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 4583. doi:
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    • Get Citation

      Brooklyn E. Taylor, Katherine Barber, Chieh Lee, Scott J Howell, Patricia R Taylor; Anti-IL-17RA enhances the efficacy of anti-VEGF. Invest. Ophthalmol. Vis. Sci. 2024;65(7):4583.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : We and others previously reported that IL-17A plays a pivotal role in VEGF production, diabetic retinopathy, and retinal neovascularization. In cancer, anti-IL-17RA increases the efficacy of anti-VEGF treatments. We hypothesized that anti-IL-17RA would increase the efficacy of anti-VEGF treatment for diabetic macular edema.

Methods : Blood of non-diabetics, Type II diabetics with diabetic macular edema that were categorized as non-responders and responders to anti-VEGF treatments was collected at Louis Stokes Cleveland VA Medical Center (n=25/group). Plasma and peripheral blood mononuclear cells (PBMC) were isolated, and protein lysates collected. Levels of IL-17A was quantified in PBMC protein lysates by ELISA. Plasma (200ml/well) was added to 10,000 human retinal endothelial cells (hREC) with or without anti-IL-17RA (IL-17A receptor antagonist) for 16h, cellular protein lysates were collected and normalized, for automated Western immunoblot analysis of vascular tight junction proteins of the retina; Zonula occludens (ZO)-1 and Vascular endothelial (VE)-Cadherin.

Results : IL-17A was not detected in the PBMC of non-diabetics, and detected in all diabetics with macular edema. The level of IL-17A was significantly higher in the anti-VEGF non-responders than responders. Additionally, tight junction proteins ZO-1 and VE-Cadherin was significantly decreased in human retinal endothelial cells (hREC) that were incubated with plasma of diabetics with macular edema when compared to hREC incubated with plasma of non-diabetics. When hREC were treated with anti-VEGF prior to plasma incubation, ZO-1 and VE-Cadherin degradation was significantly decreased in hREC incubated with plasma of anti-VEGF responders but not in hREC incubated with plasma of anti-VEGF non-responders. However, when hREC were incubated with anti-IL-17RA prior to anti-VEGF, and incubated with plasma of nondiabetics or anti-VEGF non-responders, ZO-1 and VE-Cadherin degradation in the hREC incubated with plasma of anti-VEGF non-responders was very similar (not significantly different) than hREC incubated with plasma of non-diabetic controls.

Conclusions : These results provide evidence that anti-IL-17RA enhances the efficacy of anti-VEGF treatment for diabetic macular edema. Further, our results suggest that anti-IL-17RA could be a good candidate therapeutic for diabetics with macular edema that do not respond to anti-VEGF treatment.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

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