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NFκB-Pim-1-Eomesodermin axis is critical for maintaining CD8 T-cell memory quality.

Karin M Knudson1,2, Curtis J Pritzl1, Vikas Saxena1

  • 1Department of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, MO 65212.

Proceedings of the National Academy of Sciences of the United States of America
|February 15, 2017
PubMed
Summary

Maintaining CD8 T-cell memory requires continuous NFκB signaling, which controls Eomesodermin (Eomes) expression via PIM-1 kinase. This pathway is crucial for long-term immune memory persistence and function.

Keywords:
CD8 T-cell memoryEomesoderminNFkBPim-1

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Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Biology

Background:

  • T-cell memory is essential for adaptive immunity.
  • Factors maintaining T-cell memory persistence, function, and phenotype are not fully understood.
  • Eomesodermin (Eomes) plays a role in establishing the memory T-cell pool.

Purpose of the Study:

  • To elucidate the molecular mechanisms regulating T-cell memory maintenance.
  • To investigate the role of NFκB signaling and Eomesodermin in CD8 T-cell memory.
  • To identify upstream regulators of Eomes expression in memory T cells.

Main Methods:

  • Analysis of Eomesodermin (Eomes) expression in transitioning T cells.
  • Investigating the role of NFκB signaling in memory T-cell maintenance.
  • Studying the regulation of NFκB by T-cell receptor (TCR) signaling via PIM-1 kinase.
  • Assessing the impact of NFκB-Pim-1 pathway defects on CD8 T-cell memory.

Main Results:

  • Sustained NFκB signaling is required for high Eomes expression during T-cell memory transition.
  • Impaired NFκB signaling leads to reduced Eomes expression and defective CD8 T-cell memory maintenance.
  • TCR signaling regulates NFκB and Eomes via the NFκB-dependent kinase PIM-1.
  • Restoring TCR-dependent NFκB signaling rescued defects in memory T-cell function and Eomes expression.
  • The NFκB-Pim-1-Eomes axis is critical for maintaining memory CD8 T-cell longevity, function, and Eomes levels.

Conclusions:

  • A novel NFκB-Pim-1-Eomes signaling axis maintains CD8 T-cell memory fitness.
  • Continuous NFκB activity, regulated by TCR signaling through PIM-1, is essential for sustained Eomes expression and memory T-cell longevity.
  • Understanding this pathway offers insights into improving long-term immunity.