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The zinc-finger protein ZFYVE1 modulates TLR3-mediated signaling by facilitating TLR3 ligand binding.

Abstract：

:Recognition of viral dsRNA by Toll-like receptor 3 (TLR3) leads to the induction of downstream antiviral effectors and the innate antiviral immune response. Here, we identified the zinc-finger FYVE domain-containing protein ZFYVE1, a guanylate-binding protein (GBP), as a positive regulator of TLR3-mediated signaling. Overexpression of ZFYVE1 promoted the transcription of downstream antiviral genes upon stimulation with the synthetic TLR3 ligand poly(I:C). Conversely, ZFYVE1 deficiency had the opposite effect. Zfyve1-/- mice were less susceptible than wild-type mice to inflammatory death induced by poly(I:C) but not LPS. ZFYVE1 was associated with TLR3, and the FYVE domain of ZFYVE1 and the ectodomain of TLR3 were shown to be responsible for their interaction. ZFYVE1 was bound to poly(I:C) and increased the binding affinity of TLR3 to poly(I:C). These findings suggest that ZFYVE1 plays an important role in the TLR3-mediated innate immune and inflammatory responses by promoting the ligand binding of TLR3.

journal_name

Cell Mol Immunol

journal_title

Cellular & molecular immunology

authors

Zhong X,Feng L,Xu WH,Wu X,Ding YD,Zhou Y,Lei CQ,Shu HB

doi

10.1038/s41423-019-0265-6

subject

Has Abstract

pub_date

2020-07-01 00:00:00

pages

741-752

issue

7

eissn

1672-7681

issn

2042-0226

pii

10.1038/s41423-019-0265-6

journal_volume

17

pub_type

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