Fig. 2.

Putative immune signaling network in amphioxus hepatic cells. The TLR signals can induce activation of the IKK complex and NF-κB through either the MyD88-TRAF6 or TICAM-RIP1b pathway. A group of TIR domain-containing adaptors are involved in the activation and regulation of the TLR pathway. The ligands of amphioxus TLRs remain to be determined. Putative antiviral mechanisms include viral RNA recognition by DExD/H-box helicase domain-containing receptors (e.g., LGP2 and DDX23) and activation of the TBK1-IKKɛ complex and IRFs. The transcription factor IRF family contains nine members which constitute a dynamic feedback regulatory framework among IRFs and NF-κB. In the scheme of the oxidative burst machinery, NOX2 and p22phox are transmembrane components, while p47phox, p67phox, p40phox and Rac are cytosolic subunits that are recruited to the NOX2-p22phox on activation. This phagocytic respiratory burst machinery, through releasing a large amount of ROS into the phagosome, participates in the bactericidal process of the hepatic epithelial cells. In the putative TNF system, TNF can either activate the IKK complex and NF-κB through the TNFR-TRAF pathway, or trigger caspase-dependent apoptosis through the Death receptor (TNFR with death domain)-FADD/CRADD pathway. Amphioxus has a large number of NLRs that share similar domain architectures containing a central NOD domain, a C-terminal LRR region and various N-terminal region. However, the NLR signaling pathway is unclear and needs further study. Solid lines indicate a pathway with experimental evidence; dashed lines represent no experimental support