The Role of Immune Cell Subsets in the Development of Postoperative Cognitive Dysfunction in Surgical Patients under...

Postoperative cognitive dysfunction (POCD) affects 10-54% of surgical patients, especially the elderly. It is increasingly recognized as a major perioperative complication driven by neuroinflammatory mechanisms. While physiological postoperative inflammation supports wound healing and recovery, pathological hyperactivation of immune pathways leads to blood-brain barrier disruption, immune cell infiltration, and long-term cognitive impairment.

This review examines the contribution of innate and adaptive immune cell subsets to POCD pathogenesis. Activated microglia, infiltrating monocytes, and neutrophils initiate neuroinflammatory cascades through cytokine release, while dysregulated T-cell balance (increased Th17 cells, reduced regulatory T cells) exacerbates dysfunction. Key molecular pathways involve damage-associated molecular patterns, complement activation, and impaired neurotrophin signaling. Clinical biomarkers such as IL-6, TNF-α, and S100B show predictive value, with sensitivity of 65-85% and specificity of 75-90%. Current therapeutic strategies include dexmedetomidine, anti-inflammatory agents, and comprehensive perioperative optimization.

POCD is a frequent postoperative complication linked to immune dysregulation and neuroinflammation. Both innate and adaptive immune cells play central roles, with microglial polarization and T-cell imbalance as major drivers. Biomarkers such as IL-6, TNF-α, and S100B can support risk stratification and early intervention. Immunomodulatory therapies and perioperative optimization represent promising approaches to reduce POCD incidence and improve patient outcomes.