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. 2021 Feb 19;12:639369. doi: 10.3389/fimmu.2021.639369

Figure 1.

Figure 1

Schematic representation of innate immune mechanisms in MS and AD. Non-classical monocytes and neutrophils are expanded in peripheral blood and the higher neutrophil-lymphocyte ratio (NLR) correlates with the clinical symptoms of each disease. In addition, these cells express canonical activation markers (HLA-DR and CD11b) and release inflammatory mediators, such as pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), myeloperoxidase (MPO), and neutrophil extracellular traps (NETs). Chemokine binding stimulates monocytes and neutrophils to infiltrate the CNS by chemotaxis (mediated by CCR2 and CXCR2, respectively). Within the CNS, monocytes show impaired phagocytosis and secrete the pro-inflammatory cytokines IL-1β, TNF-α, IL-6, and IL-8, thus fueling the inflammatory response. Similarly, infiltrating neutrophils contribute to neuroinflammation and tissue damage by releasing NETs, reactive oxygen species (ROS), MPO, and matrix metal proteinases (MMPs).