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Updated: Dec 17, 2025

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization
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Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Published on: October 6, 2019

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FKBP5 Regulates RIG-I-Mediated NF-κB Activation and Influenza A Virus Infection

Wenzhuo Hao1, Lingyan Wang1, Shitao Li1

  • 1Department of Microbiology and Immunology, Tulane University, New Orleans, LA 70112, USA.

Viruses
|June 26, 2020
PubMed

Insights

FKBP5 is a novel host factor that restricts influenza A virus (IAV) infection. Its absence enhances IAV replication by disrupting RIG-I-mediated immune signaling pathways.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Influenza A virus (IAV) poses a significant global health threat.
  • Host pattern recognition receptors (PRRs), like RIG-I, detect viral RNA and activate immune signaling.
  • The precise role of FKBP5 in RIG-I signaling and IAV infection remains unclear.

Purpose of the Study:

  • To elucidate the role of FKBP5 in the host response to IAV infection.
  • To investigate the interaction between FKBP5 and the RIG-I signaling pathway.

Main Methods:

  • Utilized FKBP5 knockout models to assess IAV infection levels.
  • Investigated the binding interaction between FKBP5 and IKKα.
  • Analyzed RIG-I-mediated innate immune responses and interferon-stimulated gene (ISG) expression.

Main Results:

  • FKBP5 knockout significantly increased susceptibility to IAV infection.
  • FKBP5 was found to bind with IKKα, a key component of the NF-κB pathway.
  • FKBP5 is essential for RIG-I-induced ISG expression and innate immunity.

Conclusions:

  • FKBP5 acts as a novel anti-influenza host factor.
  • FKBP5 restricts IAV infection by promoting RIG-I-mediated NF-κB signaling activation.
Keywords:
IKKantiviralfluhost defenseimmunophilin

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