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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Lambda-Interferons Inhibit Herpes Simplex Virus Type 2 Replication in Human Cervical Epithelial Cells by Activating

Zhu Li1,2, Xuan Lu1, Yufan Zhu1

  • 1Wuhan University School of Basic Medical Sciences.

Japanese Journal of Infectious Diseases
|March 3, 2017
PubMed
Summary

Lambda-interferons (IFN-λs) effectively inhibit herpes simplex virus type 2 (HSV-2) replication in human cervical cells. This antiviral activity is mediated through the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, highlighting IFN-λs therapeutic potential.

Keywords:
JAK/STAT signaling pathwayherpes simplex virus type 2human cervical epithelial cellsinterferon-stimulated genesinterferon-λ

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Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Herpes simplex virus type 2 (HSV-2) causes significant global health issues.
  • Previous research indicated lambda-interferons (IFN-λs) inhibit HSV-2 replication in human cervical epithelial cells via Toll-like receptor 3 and retinoic acid-inducible protein I pathways.
  • The precise anti-HSV-2 mechanisms and signaling differences among IFN-λs in these cells were not fully understood.

Purpose of the Study:

  • To elucidate the mechanisms by which IFN-λs inhibit HSV-2 replication in human cervical epithelial cells.
  • To investigate the specific roles of different IFN-λs and their signaling pathways in controlling HSV-2.
  • To assess the therapeutic potential of IFN-λs against HSV-2 infections.

Main Methods:

  • Treatment of human cervical epithelial cells with various IFN-λs.
  • Assessment of HSV-2 replication inhibition and cytotoxicity.
  • Analysis of gene expression, including IFN-stimulated genes (ISGs) and pattern recognition receptors (PRRs).
  • Investigation of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway using a JAK inhibitor.

Main Results:

  • IFN-λs demonstrated potent inhibition of HSV-2 replication without causing cytotoxicity.
  • IFN-λs induced the expression of ISGs and PRRs, with IFN-λ3 showing higher induction levels.
  • Upregulation of genes involved in the JAK/STAT signaling pathway was observed.
  • Inhibition of the JAK/STAT pathway abrogated IFN-λ-mediated anti-HSV-2 activity and ISG/PRR induction.
  • HSV-2 infection did not compromise the induction of ISGs and PRRs by IFN-λs.

Conclusions:

  • IFN-λs exhibit significant therapeutic potential for treating HSV-2 infections.
  • The JAK/STAT signaling pathway is crucial for IFN-λ-mediated antiviral activity against HSV-2.
  • IFN-λs enhance the innate immune response by upregulating ISGs and PRRs, contributing to viral control.