NKG2D signaling shifts the balance of CD8 T cells from single cytokine- to polycytokine-producing effector cells

Frederick J. Kohlhapp, Jeremy A. O'Sullivan, Tamson V. Moore, Andrew Zloza*, José A. Guevara-Patiño*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

CD8 T cells play a critical role in immunity against intracellular pathogens and cancer. A primary objective of T cell-based vaccine strategies is the induction of durable and effective immune responses. Achieving this goal involves more than simply boosting the numbers of responding T cells. Of particular interest is the induction of CD8 T cells with polycytokine capability, specifically with the ability of CD8 T cells to co-produce IFNγ, TNFα and IL-2. The presence of these polycytokine-producing CD8 T cells correlates strongly with protection against foreign pathogens and cancer. Therefore, approaches capable of inducing such polyfunctional responses are needed. NKG2D engagement on CD8 T cells has been shown to result in increased effector response. However, the manner in which NKG2D engagement results in improved CD8 T cell effector response is unclear. Here we demonstrate in vitro and in vivo that NKG2D engagement by its natural ligand, Rae-1ε, shifts the balance from single cytokine to polycytokine (IL-2, IFNγ, and TFNα) production. These data define a previously unrecognized process in which NKG2D costimulation on CD8 T cells results in improved effector responses.

Original languageEnglish (US)
Pages (from-to)1-6
Number of pages6
JournalMolecular Immunology
Volume155
DOIs
StatePublished - Mar 2023

Keywords

  • CD8 T cells
  • Effector function
  • NKG2D
  • Polycytokine

ASJC Scopus subject areas

  • Molecular Biology
  • Immunology

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