Unravelling the therapeutic potential of IL-33 for atrophic AMD.

Alison J Clare, Jian Liu, Sofia Theodoropoulou, Andrew David Dick*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

5 Citations (Scopus)
84 Downloads (Pure)


Age-related macular degeneration (AMD), a degenerative disease affecting the retinal pigment epithelium (RPE) and photoreceptors in the macula, is the leading cause of central blindness in the elderly. AMD progresses to advanced stages of disease, atrophic AMD (aAMD) or in 15% of cases “wet” or neovascular AMD (nAMD), associated with substantial vision loss. Whilst there has been advancement in therapies treating nAMD, to date there are no licenced effective treatments for the 85% affected by aAMD, with disease managed by changes to diet, vitamin supplements and regular monitoring. AMD has a complex pathogenesis involving highly integrated and common age-related disease pathways, including dysregulated complement/inflammation, impaired autophagy and oxidative stress. The intricacy of AMD pathogenesis makes therapeutic development challenging and identifying a target that combats the converging disease pathways is essential to provide a globally effective treatment. Interleukin-33 is a cytokine, classically known for the pro-inflammatory role it plays in allergic disease. Recent evidence across degenerative and inflammatory disease conditions reveals a diverse immune modulatory role for IL-33, with promising therapeutic potential. Here, we will review IL-33 function in disease and discuss the future potential for this homeostatic cytokine in treating AMD.
Original languageEnglish
Early online date16 Sept 2021
Publication statusPublished - 16 Sept 2021

Bibliographical note

Funding Information:
Data included in this review paper were supported by grants from the Academy of Medical Sciences (ST and ADD), GOAP Bayer award (ST) and Elizabeth Blackwell Institute Wellcome Trust (ADD).

Publisher Copyright:
© 2021, The Author(s).


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