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The impact of KLF2 modulation on the transcriptional program and function of CD8 T cells

Gavin C Preston1, Carmen Feijoo-Carnero, Nick Schurch

  • 1Department of Cell Signalling & Immunology, College of Life Sciences, University of Dundee, Dundee, United Kingdom.

Plos One
|October 25, 2013
PubMed

Insights

Krüppel-like factor 2 (KLF2) downregulation is crucial for CD8 T cells to express CXCR3 and expand. KLF2 acts as a tunable switch, modulating T cell responses based on its expression level.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Krüppel-like factor 2 (KLF2) is a transcription factor highly expressed in quiescent T lymphocytes.
  • KLF2 expression decreases in effector T cells.

Purpose of the Study:

  • To investigate the role of KLF2 downregulation in CD8 effector T cell function.
  • To determine how antigen receptor engagement affects KLF2 expression.
  • To elucidate the impact of KLF2 loss on the CD8 T cell transcriptional program.

Main Methods:

  • Studied the graded downregulation of KLF2 expression in response to T cell receptor (TCR) ligand affinity.
  • Analyzed the integrated activation of protein kinase B and MAP kinases ERK1/2.
  • Investigated the role of KLF2 loss in CD8 T cell expression of CXCR3 and clonal expansion.

Main Results:

  • Antigen receptor engagement downregulates KLF2 in a graded manner.
  • Loss of KLF2 is essential for CD8 T cells to express the inflammatory chemokine receptor CXCR3.
  • KLF2 loss is required for maximal clonal expansion of T cells.
  • KLF2 negatively controls CD8 T cell responses to the CXCR3 ligand CXCL10.
  • Distinct KLF2 thresholds exist for restraining CXCR3 expression versus T cell proliferation.

Conclusions:

  • KLF2 acts as a tunable, analogue switch rather than a digital on/off switch in T cells.
  • The magnitude of KLF2 expression differentially modulates CD8 T cell responses, including CXCR3 expression and proliferation.

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