Background: Thyroid Eye Disease [TED], also known as Graves' orbitopathy, is an autoimmune disorder marked by orbital inflammation and tissue remodeling. Interleukin-8 [IL-8], a pro-inflammatory cytokine, is increasingly recognized as crucial in TED's pathogenesis and progression. This review explores IL-8's role in TED, focusing on its contributions to inflammation, tissue remodeling, and fibrosis, and examines emerging therapies targeting IL-8 signaling.
Summary and Conclusion: A detailed analysis was conducted on IL-8's role in TED pathophysiology, emphasizing its impact on orbital inflammation, adipogenesis, angiogenesis, fibrosis, and hyaluronan production. Recent therapeutic advances targeting IL-8 were reviewed for their potential benefits in TED management. Results: IL-8 significantly contributes to TED by amplifying inflammation through immune cell recruitment and activation in orbital tissues. It promotes adipogenesis by facilitating pre-adipocyte differentiation, leading to orbital adipose tissue expansion. IL-8 drives angiogenesis, enhances vascularization, and exacerbates tissue damage. It also stimulates fibroblast activation and extracellular matrix deposition, contributing to fibrosis and tissue remodeling. Additionally, IL-8 increases hyaluronan production, causing tissue swelling and worsening TED symptoms. Therapeutic approaches inhibiting IL-8 signaling show promise in reducing inflammation and pathological tissue changes in TED. IL-8 is a key mediator of inflammation and tissue remodeling in TED, making it a promising therapeutic target. Targeting IL-8 signaling pathways offers a novel approach for TED management, though further research is needed to optimize treatments and understand the broader implications of IL-8 modulation in this disease.