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<p>The Bruton’s kinase inhibitor ibrutinib has become a cornerstone in the treatment of chronic lymphocytic leukemia (CLL). Previous studies reported an association between upregulation of TCF1 and BCL11B transcription factors with favorable survival outcomes in CLL patients. This study aimed to investigate the correlation of TCF1 and BCL11B with response to ibrutinib. Four GEO databases were used to examine the transition of CD8 + T cell subsets and the expression of TCF1 and BCL11B in CLL patients undergoing ibrutinib treatment, and the findings were validated in a cohort of 98 CLL patients. Briefly, ibrutinib treatment increased the proportion of effector T cell-like (Teff-like) cells and upregulated TCF1 and BCL11B in CD8 + T cells. We identified a subset of TCF1 + BCL11B+ Teff-like cells with high cytotoxic activity score that were almost undetectable prior to treatment but started to emerge following ibrutinib treatment. Importantly, these changes correlated with favorable response to ibrutinib, where chromatin accessibilities of <i>TCF7 (encoding</i> TCF1<i>)</i> and <i>BCL11B</i> were increased and TCF1 interacted with BCL11B to restore T cell immunity, but not in patients with poor response to ibrutinib. These findings suggest that the emergence and increase of BCL11B + TCF1 + CD8+ Teff cells likely reflect reconstitution of T cell immunity induced by ibrutinib.</p>

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Upregulation of TCF1 and BCL11B in CD8+ effector T cells predicts favorable response to ibrutinib in patients with chronic lymphocytic leukemia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月8日

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  • Ge Liu,
  • Taotao Liang,
  • Hao Ai,
  • Shan Wang,
  • Songke Yin,
  • Xiaojiao Wang,
  • Hongfei Wu,
  • Qian Wang,
  • Hongmian Zhao,
  • Xiaojuan Liu,
  • Xiaodong Luv,
  • Jia Liu,
  • Qingsong Yin

摘要

The Bruton’s kinase inhibitor ibrutinib has become a cornerstone in the treatment of chronic lymphocytic leukemia (CLL). Previous studies reported an association between upregulation of TCF1 and BCL11B transcription factors with favorable survival outcomes in CLL patients. This study aimed to investigate the correlation of TCF1 and BCL11B with response to ibrutinib. Four GEO databases were used to examine the transition of CD8 + T cell subsets and the expression of TCF1 and BCL11B in CLL patients undergoing ibrutinib treatment, and the findings were validated in a cohort of 98 CLL patients. Briefly, ibrutinib treatment increased the proportion of effector T cell-like (Teff-like) cells and upregulated TCF1 and BCL11B in CD8 + T cells. We identified a subset of TCF1 + BCL11B+ Teff-like cells with high cytotoxic activity score that were almost undetectable prior to treatment but started to emerge following ibrutinib treatment. Importantly, these changes correlated with favorable response to ibrutinib, where chromatin accessibilities of TCF7 (encoding TCF1) and BCL11B were increased and TCF1 interacted with BCL11B to restore T cell immunity, but not in patients with poor response to ibrutinib. These findings suggest that the emergence and increase of BCL11B + TCF1 + CD8+ Teff cells likely reflect reconstitution of T cell immunity induced by ibrutinib.