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IFITM3 restricts virus-induced inflammatory cytokine production by limiting Nogo-B mediated TLR responses

Abstract:
Interferon-induced transmembrane protein 3 (IFITM3) is a restriction factor that limits viral pathogenesis and exerts poorly understood immunoregulatory functions. Here, using human and mouse models, we demonstrate that IFITM3 promotes MyD88-dependent, TLR-mediated IL-6 production following exposure to cytomegalovirus (CMV). IFITM3 also restricts IL-6 production in response to influenza and SARS-CoV-2. In dendritic cells, IFITM3 binds to the reticulon 4 isoform Nogo-B and promotes its proteasomal degradation. We reveal that Nogo-B mediates TLR-dependent pro-inflammatory cytokine production and promotes viral pathogenesis in vivo, and in the case of TLR2 responses, this process involves alteration of TLR2 cellular localization. Nogo-B deletion abrogates inflammatory cytokine responses and associated disease in virus-infected IFITM3-deficient mice. Thus, we uncover Nogo-B as a driver of viral pathogenesis and highlight an immunoregulatory pathway in which IFITM3 fine-tunes the responsiveness of myeloid cells to viral stimulation.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41467-022-32587-4

Authors

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Role:
Author
ORCID:
0000-0002-9280-5281
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Institution:
University of Oxford
Division:
MSD
Department:
RDM
Sub department:
Weatherall Insti. of Molecular Medicine
Role:
Author


Publisher:
Springer Nature
Journal:
Nature Communications More from this journal
Volume:
13
Issue:
1
Article number:
5294
Publication date:
2022-09-08
Acceptance date:
2022-08-08
DOI:
EISSN:
2041-1723
Pmid:
36075894


Language:
English
Keywords:
Pubs id:
1278428
Local pid:
pubs:1278428
Deposit date:
2022-09-26
ARK identifier:

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