Fig. 6Figure 6
Peripheral immune cell trafficking and interactions in Alzheimer’s disease (AD). In AD, blood-brain barrier (BBB) disruption, accompanied by increased vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule 1 (ICAM-1) expression, facilitates immune infiltration. Major cell types include: (1) monocytes/macrophages with impaired phagocytosis and dysregulated pro-inflammatory/repair-associated microglia polarization; (2) dendritic cells engaged in amyloid-β (Aβ) clearance and antigen presentation; (3) T cells, pro-inflammatory Th1/Th17, regulatory Tregs, and cytotoxic CD8+; (4) B cells producing Aβ-targeting antibodies and inflammatory cytokines; (5) natural killer (NK) cells with heightened interferon-γ (IFN-γ) and tumor necrosis factor alpha (TNF-α) release; and (6) neutrophils releasing reactive oxygen species (ROS), proteases, and forming neutrophil extracellular traps (NETs). Lymphatic drainage to cervical nodes and chemokine gradients, i.e., C-C motif chemokin