Immune inflammatory targets and anti-inflammatory therapy in dry eye disease.

Abstract

Background: Dry eye disease (DED) is a common category of ocular surface disease caused by insufficient tear secretion or reduced tear film quality, which leads to damage to ocular surface epithelial cells and initiates an inflammatory response, ultimately forming a vicious cycle dominated by chronic inflammation. The signaling pathways involved in DED are complex and need to be further explored.

Methods: A literature search of PubMed was conducted to identify studies on DED published between 2013 and 2026.The search strategy adopted a combination of keywords as follows: "dry eye disease", "neuroimmune and inflammation", "inflammatory signaling pathway", "ocular surface microenvironment. Inclusion Criteria": 1.Original human clinical trials, in vitro cellular experiments, and animal model studies related to DED;2. Systematic reviews focusing on immunity and inflammation in DED.

Exclusion criteria: 1. Studies solely addressing other ocular surface diseases such as conjunctivitis, keratitis, and uveitis; 2. Studies lacking experimental data supporting anti-inflammatory therapeutic effects.

Results: Previous studies have shown that anti-inflammatory therapies hold great promise for the treatment of moderate to severe DED. Inhibiting T cell activation or the release of inflammatory cytokines can help break the vicious cycle of inflammation. The NF-κB pathway plays a central role in the pathogenesis of DED.

Conclusions: Chronic inflammation can continuously damage epithelial cells, exacerbating the severity of DED and significantly impacting the patient's quality of life. Therefore, understanding the underlying inflammatory mechanisms is crucial for the development of effective therapeutic strategies for DED.