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. 2022 Jul 14;13:891328. doi: 10.3389/fimmu.2022.891328

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Copyright © 2022 Xu, Li and Huang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Signal transduction initiated by TL1A/DR3. TL1A binds to the receptor DR3 and activates the TRADD pathway. The complex exerts pro-inflammatory effects by regulating downstream pathways, such as TRAF2, RIP1, PI3K, MAPKs, NF-κB, and then regulates cytokine, chemokine secretion. TL1A/DR3 is involved in promoting apoptosis and necroptotic cell death through FADD, RIP3, Caspase-8/-3/-7 pathways. NF-κB can activate c-IAP protein, which can negatively regulate apoptosis. TRADD, TNFR-associated death domain protein; TRAF2, TNFR-associated factor 2; RIP1, receptor-interacting protein 1; PI3K, phosphatidylinositol 3-kinase; MAPKs, mitogen-activated protein kinases; NF-κB, nuclear factor kappa B; FADD, fas-associated death domain; RIP3, receptor-interacting protein 3; c-IAP, cellular inhibitor of apoptosis proteins.