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Fine-Tuning of CD8(+) T Cell Mitochondrial Metabolism by the Respiratory Chain Repressor MCJ Dictates Protection to

Devin P Champagne1, Ketki M Hatle1, Karen A Fortner1

  • 1Program in Immunobiology, Department of Medicine, University of Vermont, Burlington, Vermont, 05405 USA.

Immunity
|May 29, 2016
PubMed

Insights

Methylation-controlled J protein (MCJ) regulates mitochondrial respiration in CD8(+) T cells. MCJ deficiency enhances T cell metabolism and boosts anti-viral immunity, suggesting MCJ as a therapeutic target.

Area of Science:

  • Immunology
  • Cellular Metabolism
  • Mitochondrial Biology

Background:

  • Mitochondrial respiration is crucial for CD8(+) T cell function.
  • Mechanisms regulating mitochondrial respiration during T cell differentiation are not fully understood.

Purpose of the Study:

  • To investigate the role of MCJ (methylation-controlled J protein) in regulating mitochondrial respiration in CD8(+) T cells.
  • To determine the impact of MCJ deficiency on T cell metabolism and anti-viral immunity.

Main Methods:

  • Metabolic profiling of CD8(+) T cells.
  • Analysis of electron transport chain supercomplex formation.
  • Assessment of interferon-gamma secretion.
  • Evaluation of protection against influenza virus infection in vivo.

Main Results:

  • MCJ acts as an endogenous brake on mitochondrial respiration by inhibiting electron transport chain supercomplex assembly.
  • MCJ-deficient CD8(+) T cells exhibit enhanced mitochondrial metabolism, oxidative phosphorylation, and ATP accumulation.
  • MCJ deficiency selectively increases interferon-gamma secretion and improves memory CD8(+) T cell-mediated anti-viral protection.
  • MCJ regulates effector CD8(+) T cell metabolism during the contraction phase.

Conclusions:

  • MCJ fine-tunes CD8(+) T cell mitochondrial metabolism without altering mitochondrial mass.
  • Targeting MCJ offers a potential strategy to enhance CD8(+) T cell-mediated immune responses.

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