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. 2024 Aug 9;15:1423069. doi: 10.3389/fimmu.2024.1423069

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Copyright © 2024 Liao, Mao, Wang, Wang, Ocansey, Wang and Mao

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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Key signaling pathways associated with IBD ① TLR stimulation triggers MyD88 to interact with IRAK4 (interleukin-1 receptor-associated kinase 4) and ② NLRs interact with RIP2, causing TRAF3, TRAF6, and Lys63 polyubiquitinizes RIP1, to recruit TAK1/TAB2/3 complex or IkK complex. This triggers the activation of NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways, promoting the transcription of proinflammatory and anti-inflammatory genes. Endosomal TLRs transmit signals through a TRIF-dependent pathway, and TRIF, along with RIP1 and TRAF3, activates TAK1 or IKKϵ, leading to phosphorylation of IRF3 and expression of interferon β.