Wdfy1 deficiency impairs Tlr3-mediated immune responses in vivo
Wdfy1 deficiency impairs Tlr3-mediated immune responses in vivo
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DOI：
10.1038/s41423-020-0461-4
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发表时间：
2020
影响因子：
24.1
通讯作者：
Liu Yu
中科院分区：
文献类型：
--
作者：
Yang Yang;Hu Yunhong;Liu Yu
As germline-encoded pattern recognition receptors, Toll-like receptors (TLRs) play important roles in innate immune responses against various pathogens.1 Among TLR family members, only TLR3 and TLR4 use TIR domain-containing adapter-inducing interferon-β (TRIF) as an adapter protein to trigger the production of type I interferon (IFN-I) and inflammatory cytokines.1,2 Secreted IFNs then bind their plasma membrane receptors, further stimulating the transcription of IFN-stimulated genes (ISGs), which have multiple antiviral functions, such as restricting the replication and assembly of viral particles.3 We previously reported an accessory protein, named WD repeat and FYVE domain-containing protein (WDFY1), that strengths the interaction between TRIF and TLR3 or TLR4.4 At the cellular level, overexpression of WDFY1 reinforced TLR3/4-mediated innate immune responses, and the suppression of WDFY1 by RNAi had the opposite effects. We also reported that the function of WDFY1 is highly dependent on its FYVE domain, which is responsible for its localization to the early endosome.5 However, whether Wdfy1-knockout (KO) mice are susceptible to Tlr3 or Tlr4 ligands remains unknown.
