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Updated: Feb 13, 2026

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Cytoskeletal Prestress Regulates RIG-I-Mediated Innate Immunity.

Arpan Roy1, Sydney Sarver1, Jarod Beights2,3

  • 1School of Mechanical, Aerospace, and Materials Engineering, Southern Illinois University Carbondale, Carbondale, IL 62901, USA.

Biophysica
|February 12, 2026
PubMed
Summary
This summary is machine-generated.

Cell stiffness regulates innate immunity. Cells on soft surfaces show reduced antiviral responses due to cytoskeletal prestress impacting RIG-I signaling, while stiff surfaces enhance it.

Keywords:
RIG-ITBK1YAPcytoskeletal prestresstraction

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Area of Science:

  • Immunology
  • Cell Biology
  • Biophysics

Background:

  • Innate immunity provides crucial antiviral defense via signaling pathways like retinoic acid-inducible gene I (RIG-I).
  • The influence of cytoskeletal prestress, a key aspect of cellular mechanotransduction, on RIG-I signaling and innate immunity is not well understood.

Purpose of the Study:

  • To investigate the role of cytoskeletal prestress in regulating RIG-I signaling and type-I interferon (IFN) gene expression.
  • To determine how substrate stiffness affects innate immune responses.

Main Methods:

  • Cells were cultured on soft (0.6 kPa) and stiff (8.5 kPa) substrates to alter cellular traction and prestress.
  • Poly(I:C), a viral dsRNA mimic, was used to stimulate the RIG-I pathway.
  • Expression of IFN-β1 and IFN-stimulated genes (ISGs) was measured.
  • The activation and localization of TANK Binding Kinase 1 (TBK1) and Yes-associated protein (YAP) were assessed.

Main Results:

  • Cells on soft substrates exhibited minimal RIG-I signaling activation and low IFN-β1 and ISG expression.
  • On soft substrates, YAP localized to the cytoplasm, inhibiting TBK1 activation.
  • Cells on stiff substrates showed enhanced RIG-I signaling, elevated TBK1 activation, and increased IFN and ISG expression due to nuclear YAP localization.

Conclusions:

  • Cytoskeletal prestress significantly influences the activation of RIG-I signaling and subsequent innate immune responses.
  • Substrate stiffness, by modulating cytoskeletal prestress and YAP localization, acts as a critical biophysical regulator of antiviral signaling.