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Regulation of Mitochondria-Derived Immune Activation by 'Antiviral' TRIM Proteins

Seeun Oh1, Michael A Mandell1,2

  • 1Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.

Viruses
|July 27, 2024
PubMed

Insights

Tripartite motif-containing (TRIM) proteins regulate mitochondria's role in innate immunity and antiviral defense. They control mitochondrial immune signals and mitophagy, impacting inflammation and disease.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Mitochondria are crucial for innate immune responses and antiviral signaling.
  • Mitochondria can release immune-stimulatory molecules, boosting interferon production during viral infections.
  • Damaged mitochondria can inappropriately trigger immune responses, mimicking antiviral reactions.

Purpose of the Study:

  • To review the role of tripartite motif-containing (TRIM) proteins in regulating mitochondria-based innate immune activation.
  • To explore how TRIMs modulate mitochondrial immune signaling and mitophagy in antiviral defense.
  • To understand TRIMs' broader implications in diseases linked to mitochondrial inflammation.

Main Methods:

  • Literature review focusing on TRIM proteins and mitochondrial antiviral immunity.
  • Analysis of TRIM protein functions in immune signal transduction pathways.
  • Examination of TRIMs' role in mitophagy and removal of mitochondrial factors.

Main Results:

  • TRIM proteins are essential for antiviral defense and regulate mitochondria-mediated innate immunity.
  • TRIMs modulate immune-signaling pathways activated by mitochondrial molecules.
  • TRIMs coordinate mitophagy to remove mitochondria and associated immune-activating factors.

Conclusions:

  • TRIM proteins have dual roles in innate immunity: antiviral defense and regulation of mitochondria-based inflammation.
  • TRIMs' functions in controlling mitochondrial immune activation broaden their known roles.
  • Dysregulation of TRIMs may contribute to diseases associated with mitochondria-derived inflammation.
Keywords:
MAVSMDA5RIG-ISTINGTBK1TRIMantiviral defenseautophagycGASinflammationinterferonmitochondriamitophagyrestriction factortripartite motif

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