Degradation of IKZF1 prevents epigenetic progression of T cell exhaustion in an antigen-specific assay

Cell Rep Med. 2024 Nov 19;5(11):101804. doi: 10.1016/j.xcrm.2024.101804. Epub 2024 Oct 31.

Abstract

In cancer, chronic antigen stimulation drives effector T cells to exhaustion, limiting the efficacy of T cell therapies. Recent studies have demonstrated that epigenetic rewiring governs the transition of T cells from effector to exhausted states and makes a subset of exhausted T cells non-responsive to PD1 checkpoint blockade. Here, we describe an antigen-specific assay for T cell exhaustion that generates T cells phenotypically and transcriptionally similar to those found in human tumors. We perform a screen of human epigenetic regulators, identifying IKZF1 as a driver of T cell exhaustion. We determine that the IKZF1 degrader iberdomide prevents exhaustion by blocking chromatin remodeling at T cell effector enhancers and preserving the binding of AP-1, NF-κB, and NFAT. Thus, our study uncovers a role for IKZF1 as a driver of T cell exhaustion through epigenetic modulation, providing a rationale for the use of iberdomide in solid tumors to prevent T cell exhaustion.

MeSH terms

  • Chromatin Assembly and Disassembly
  • Epigenesis, Genetic*
  • Humans
  • Ikaros Transcription Factor* / genetics
  • Ikaros Transcription Factor* / metabolism
  • NF-kappa B / metabolism
  • NFATC Transcription Factors / genetics
  • NFATC Transcription Factors / metabolism
  • Neoplasms / genetics
  • Neoplasms / immunology
  • Neoplasms / pathology
  • T-Cell Exhaustion
  • T-Lymphocytes* / immunology
  • T-Lymphocytes* / metabolism
  • Transcription Factor AP-1 / metabolism

Substances

  • Ikaros Transcription Factor
  • IKZF1 protein, human
  • NF-kappa B
  • Transcription Factor AP-1
  • NFATC Transcription Factors