Sox4 represses host innate immunity to facilitate pathogen infection by hijacking the TLR signaling networks Article Swipe
Jian Shang
,
Yuan Zheng
,
Jiayin Mo
,
Wenbiao Wang
,
Zhen Luo
,
Yongkui Li
,
Xulin Chen
,
Qiwei Zhang
,
Kailang Wu
,
Weiyong Liu
,
Jianguo Wu
·
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1080/21505594.2021.1882775
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.1080/21505594.2021.1882775
Toll-like receptors (TLRs) are essential for the protection of the host from pathogen infections by initiating the integration of contextual cues to regulate inflammation and immunity. However, without tightly controlled immune responses, the host will be subjected to detrimental outcomes. Therefore, it is important to balance the positive and negative regulations of TLRs to eliminate pathogen infection, yet avert harmful immunological consequences. This study revealed a distinct mechanism underlying the regulation of the TLR network. The expression of sex-determining region Y-box 4 (Sox4) is induced by virus infection in viral infected patients and cultured cells, which subsequently represses the TLR signaling network to facilitate viral replication at multiple levels by a distinct mechanism. Briefly, Sox4 inhibits the production of myeloid differentiation primary response gene 88 (MyD88) and most of the TLRs by binding to their promoters to attenuate gene transcription. In addition, Sox4 blocks the activities of the TLR/MyD88/IRAK4/TAK1 and TLR/TRIF/TRAF3/TBK1 pathways by repressing their key components. Moreover, Sox4 represses the activation of the nuclear factor kappa-B (NF-κB) through interacting with IKKα/α, and attenuates NF-kB and IFN regulatory factors 3/7 (IRF3/7) abundances by promoting protein degradation. All these contributed to the down-regulation of interferons (IFNs) and IFN-stimulated gene (ISG) expression, leading to facilitate the viral replications. Therefore, we reveal a distinct mechanism by which viral pathogens evade host innate immunity and discover a key regulator in host defense.
Related Topics
Concepts
Biology
Innate immune system
TRIF
Transcription factor
IRF3
TANK-binding kinase 1
Cell biology
Immunology
SOX4
Immunity
Signal transduction
Immune system
Toll-like receptor
Gene
Promoter
Gene expression
Genetics
Protein kinase C
Mitogen-activated protein kinase kinase
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1080/21505594.2021.1882775
- https://www.tandfonline.com/doi/pdf/10.1080/21505594.2021.1882775?needAccess=true
- OA Status
- gold
- Cited By
- 19
- References
- 56
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3127586740
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W3127586740Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1080/21505594.2021.1882775Digital Object Identifier
- Title
-
Sox4 represses host innate immunity to facilitate pathogen infection by hijacking the TLR signaling networksWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2021Year of publication
- Publication date
-
2021-02-01Full publication date if available
- Authors
-
Jian Shang, Yuan Zheng, Jiayin Mo, Wenbiao Wang, Zhen Luo, Yongkui Li, Xulin Chen, Qiwei Zhang, Kailang Wu, Weiyong Liu, Jianguo WuList of authors in order
- Landing page
-
https://doi.org/10.1080/21505594.2021.1882775Publisher landing page
- PDF URL
-
https://www.tandfonline.com/doi/pdf/10.1080/21505594.2021.1882775?needAccess=trueDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://www.tandfonline.com/doi/pdf/10.1080/21505594.2021.1882775?needAccess=trueDirect OA link when available
- Concepts
-
Biology, Innate immune system, TRIF, Transcription factor, IRF3, TANK-binding kinase 1, Cell biology, Immunology, SOX4, Immunity, Signal transduction, Immune system, Toll-like receptor, Gene, Promoter, Gene expression, Genetics, Protein kinase C, Mitogen-activated protein kinase kinaseTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
19Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 4, 2024: 6, 2023: 4, 2022: 4, 2021: 1Per-year citation counts (last 5 years)
- References (count)
-
56Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| publication_year | 2021 |
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