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The interplay between classical and alternative isoprenoid biosynthesis controls gammadelta T cell bioactivity of

Máire Begley1, Cormac G M Gahan, Ann-Kristin Kollas

  • 1Department of Microbiology and Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland.

FEBS Letters
|March 12, 2004
PubMed

Insights

Listeria monocytogenes utilizes both mevalonate and MEP pathways for isoprenoid synthesis. Disrupting one pathway complements the other, impacting T cell activation via HMB-PP accumulation.

Area of Science:

  • Microbiology
  • Immunology
  • Biochemistry

Background:

  • Isoprenoids are vital molecules synthesized via the mevalonate or MEP pathways.
  • The MEP pathway intermediate HMB-PP activates human Vgamma9/Vdelta2 T cells.
  • Listeria monocytogenes uniquely possesses both isoprenoid biosynthesis pathways.

Purpose of the Study:

  • To investigate the functional interplay between the mevalonate and MEP pathways in Listeria monocytogenes.
  • To determine the impact of these pathways on HMB-PP production and T cell activation.

Main Methods:

  • Employing strategic gene knockouts in Listeria monocytogenes to disrupt specific isoprenoid pathways.
  • Analyzing the compensatory expression of the MEP pathway upon mevalonate pathway disruption.
  • Assessing Vgamma9/Vdelta2 T cell bioactivity in response to bacterial mutants with altered HMB-PP levels.

Main Results:

  • Both mevalonate and MEP pathways are functional but not essential for Listeria monocytogenes viability.
  • Disruption of the mevalonate pathway leads to a compensatory upregulation of the MEP pathway.
  • Mutants accumulating HMB-PP showed increased Vgamma9/Vdelta2 T cell activity, while those unable to produce HMB-PP lost this activity.

Conclusions:

  • Listeria monocytogenes exhibits metabolic plasticity in isoprenoid synthesis, balancing pathway usage.
  • The MEP pathway's HMB-PP is a key factor in activating human Vgamma9/Vdelta2 T cells during Listeria infection.
  • Targeting these pathways could offer novel strategies for modulating host immune responses against microbial pathogens.

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