Sensorineural hearing loss (SNHL) is a highly prevalent sensory disorder globally, affecting over 1.5 billion people, with a growing societal burden exacerbated by population aging. Traditional research has focused on direct damage mechanisms to hair cells and spiral ganglion neurons, while current hearing assistive devices cannot achieve biological repair. Recent research paradigms have shifted from a “single-cell injury” perspective to a systemic view of the “neuro-immune-vascular” unit, revealing that the cochlea is not an immune-privileged site but rather a highly dynamic immune microenvironment. This immune microenvironment plays a core, dual-role in maintaining inner ear homeostasis and injury response: moderate inflammation aids repair, whereas uncontrolled inflammation exacerbates secondary damage. This review systematically summarizes the regulatory mechanisms of the cochlear immune microenvironment in the pathogenesis of SNHL, with a focus on the phenotypic plasticity of resident macrophages, infiltration of peripheral immune cells, the immunomodulatory role of glial cells, and key signaling pathways such as Nuclear Factor kappa B (NF-κB) and the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome. Concurrently, it evaluates advances in research technologies like single-cell transcriptomics and animal models, and discusses potential precision therapeutic strategies targeting the immune microenvironment (e.g., intervening specific pathways, reprogramming immune cells, combining nanodelivery systems), and considers the influence of sex as a biological variable on immune responses, aiming to provide new insights for promoting inner ear repair and advancing personalized medicine.
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