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Cyclin-dependent kinase 5 negatively regulates antiviral immune response by disrupting myeloid differentiation primary response protein 88 self-association.
Ren, Jian-Ping; Cong, Hao-Long; Gao, Li-Jie; Jiang, Dong-Fang; Li, Xin-Tong; Wang, Yun; Wang, Jiu-Qiang; Tang, Tie-Shan.
Afiliação
  • Ren JP; State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
  • Cong HL; University of Chinese Academy of Sciences, Beijing, China.
  • Gao LJ; Beijing Institute for Stem Cell and Regenerative Medicine, Beijing, China.
  • Jiang DF; Chinese Academy of Inspection and Quarantine, Beijing, China.
  • Li XT; State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
  • Wang Y; University of Chinese Academy of Sciences, Beijing, China.
  • Wang JQ; Beijing Institute for Stem Cell and Regenerative Medicine, Beijing, China.
  • Tang TS; State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Virulence ; 14(1): 2223394, 2023 12.
Article em En | MEDLINE | ID: mdl-37332205
As a member of the pattern recognition receptors (PRRs) involving in the innate immune system, Toll-like receptors (TLRs) can sense a wide range of microbial pathogens and combat infections by producing antimicrobial products, inflammatory cytokines, and chemokines. All TLRs, with the exception of TLR3, activate a signalling cascade via the myeloid differentiation primary response gene 88 (MyD88). Therefore, the activation of MyD88-dependent signalling pathway must be finely controlled. Herein, we identified that cyclin-dependent kinase 5 (CDK5) negatively regulated TLR-MyD88 signalling pathway by targeting MyD88. Overexpression of CDK5 reduced the production of interferons (IFNs), while a deficiency in CDK5 increased the expression of IFNs in response to vesicular stomatitis virus (VSV) infection. Mechanistically, CDK5 suppressed the formation of MyD88 homodimers, resulting in the attenuated production of IFNs induced by VSV infection. Surprisingly, its kinase activity does not play a role in this process. Therefore, CDK5 can act as an internal regulator to prevent excessive production of IFNs by restricting TLR-MyD88-induced activation of antiviral innate immunity in A549 cells.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Viroses / Fator 88 de Diferenciação Mieloide Tipo de estudo: Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Viroses / Fator 88 de Diferenciação Mieloide Tipo de estudo: Prognostic_studies / Risk_factors_studies Idioma: En Ano de publicação: 2023 Tipo de documento: Article