Immuno-inflammatory axis of menopausal dry eye: from hormonal fluctuations to ocular surface dysregulation.

Menopause is a significant risk factor for dry eye disease (DED), conventionally explained by estrogen deficiency and diminished tear production. Recent evidence, however, highlights the pivotal role of immune-inflammatory mechanisms in its development. This mini-review aims to integrate contemporary insights into the immuno-inflammatory pathways active in menopausal DED, clarifying how variations in sex hormones initiate and perpetuate immune dysregulation within the ocular surface microenvironment. We propose that menopausal DED is not solely a disorder of inadequate lubrication but rather a chronic immune-mediated inflammatory state, propelled by hormonal shifts. Its pathology is defined by a self-sustaining cycle of T cell-led inflammation, loss of goblet cells, and neurosensory dysfunction, which together exacerbate ocular surface impairment and clinical symptoms.