Beneficial or Harmful Role of Macrophages in Guillain-Barré Syndrome and Experimental Autoimmune Neuritis

Figure 2

Major signaling pathways involved in M1/M2 polarization. M1 macrophage polarization is mainly induced by granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon (IFN), lipopolysaccharide (LPS), and tumor necrosis factor (TNF), which activate the Janus Kinase/signal transducer and activator of transcription/myeloid differentiation factor 88/nuclear transcription factor-κB (JAK/STAT/MyD88/NF-κB) signaling pathways, which lead to the production of proinflammatory molecules such as inducible nitric oxide synthase (iNOS), TNF-α, interleukin- (IL-) 1, and IL-6. IL-4, IL-10, IL-13, and immune complexes (IC) induce M2 macrophage polarization by activating STAT6 and phosphatidylinositide 3-kinases (PI3K) signaling pathways resulting in the upregulation of peroxisome proliferator-activated receptor- (PPAR-) δ/γ and anti-inflammatory cytokines (IL-10 and tumor growth factor (TGF)-β).