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Ceftazidime reduces cellular Skp2 to promote type-I interferon activity

Caixia Qiao1, Fan Huang1,2, Jiuyi He1

  • 1Institutes of Biology and Medical Sciences, Jiangsu Key Laboratory of Infection and Immunity, Soochow University, Suzhou, Jiangsu, China.

Immunology
|August 29, 2023
PubMed

Insights

Skp2 protein promotes viral infections by degrading the type-I interferon receptor (IFNAR2). The antibiotic ceftazidime inhibits Skp2, enhancing antiviral defenses.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Skp2 is implicated in various cellular processes and cancer.
  • Type-I interferons (IFN-I) are crucial for antiviral immunity.
  • The regulation of IFN-I signaling by Skp2 remains largely unexplored.

Purpose of the Study:

  • To investigate the role of Skp2 in IFN-I-mediated antiviral activity.
  • To identify mechanisms by which Skp2 affects IFN-I signaling.
  • To explore potential therapeutic strategies targeting Skp2 for antiviral purposes.

Main Methods:

  • Cell-based assays to assess viral infection and IFN-I signaling.
  • Co-immunoprecipitation to study protein-protein interactions.
  • Western blotting and ubiquitination assays to analyze protein degradation.
  • Treatment with ceftazidime to evaluate its effect on Skp2 and IFN-I activity.

Main Results:

  • Skp2 was found to promote viral infection.
  • Skp2 interacts with IFNAR2 and promotes its K48-linked polyubiquitination and degradation.
  • Skp2-mediated downregulation of IFNAR2 inhibits IFN-I signaling and antiviral responses.
  • Ceftazidime was identified as a novel repressor of Skp2.
  • Ceftazidime treatment enhanced IFNAR2 stability and IFN-I antiviral activity.

Conclusions:

  • Skp2 negatively regulates IFN-I-mediated antiviral activity by targeting IFNAR2 for degradation.
  • Ceftazidime emerges as a potential therapeutic agent to boost antiviral immunity by inhibiting Skp2.
Keywords:
IFNAR2Skp2innate immunityinterferonubiquitination

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