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An update on our understanding of host defense mechanisms at the ocular surface; innate immune dysregulation at the ocular surface: lessons from Stevens–Johnson syndrome and related inflammatory disorders
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DOI：10.1080/1744666X.2026.2691029.png)
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Abstract
En 中文
The ocular surface is a frontline mucosal immune barrier that protects the eye from pathogens while preserving immune tolerance essential for vision. Breakdown of this innate immune homeostasis can trigger chronic ocular surface inflammation, exemplified by Stevens–Johnson syndrome/toxic epidermal necrolysis with severe ocular complications (SJS/TEN with SOC) and atopic keratoconjunctivitis (AKC).
The review summarizes current knowledge of ocular surface innate immunity, focusing on pattern-recognition receptors (TLR3, RIG-I, MDA5) and downstream interferon-stimulated genes (e.g. IFI44L, CXCL10, IFIT2) and their regulation. The influence of host genetic predispositions and microRNA regulatory networks on these pathways is highlighted, and innate immune profiles are compared among SJS/TEN with SOC, AKC, and healthy ocular surfaces.
Dysregulation of mucosal innate immunity – shaped by host genetic factors, abnormal epithelial responses, and microRNA-mediated feedback loops – underlies the persistence and severity of chronic ocular surface disorders such as SJS/TEN with SOC and AKC. A deeper understanding of these mechanisms may inform the development of novel diagnostic biomarkers (e.g. microRNA signatures) and immune-modulating therapies to restore immune homeostasis and prevent vision-threatening inflammation. PubMed was used as the literature search methodology.
Keywords:
Ocular surface inflammation
Stevens–Johnson syndrome (SJS)
severe ocular complications (SOC)
innate immunity
miRNA
TLR3
EP3
IKZF1
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