FIGURE 2.

Activation of key signaling pathways in immune cells during inflammation response. Signal (A): In the canonical nuclear factor‐κB (NF‐κB) signaling pathway, lipopolysaccharide (LPS) activates Toll‐like receptors (TLRs), and MyD88 delivers this signaling to a serious of adaptor protein leading to activation of IκB kinase (IKK)β in IKK complex, subsequently activating phosphorylation of IκBα, which is degraded by the proteasome in further. NF‐κB (RelA and P50) homo‐ or heterodimers translocated into nucleus to regulate target genes expression, such as interleukin (IL)‐6, interferons (IFNs). Signal (B): Type Ⅰ IFN activate canonical signaling pathways leading JAK/STAT cascades signaling transduction. ISGF3 complex is formed by IRF9 and phosphorylation STAT1 STAT2, activating downstream targeting genes interferon‐stimulated genes (ISGs) (examples, IL‐17, IL‐10) after transporting into the nucleus. Signal (C): In the canonical NLRP3 (Nod‐like receptor family pyrin domain containing 3) inflammasome pathway, expression of NLRP3 is regulated by MyD88–NF‐κB pathway. Once activation, NLRP3 undergoes oligomerization, recruit ASC (apoptosis‐associated speck‐like protein containing CARD) and pro‐caspase‐1 to assemble NLRP3 inflammasome, which induces caspase activation and IL‐1β, IL‐18 maturation. These cytokines promote inflammatory responses in target tissues (created with BioRender.com).