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BATF3 regulates differentiation of CD8+ T lymphocytes and memory differentiation program
Koji Umemura1, Yasuhiro Kojima2, Jakrawadee Julamanee1,3
1Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Life Science Alliance
|April 13, 2026
Summary
Basic Leucine Zipper ATF-Like Transcription Factor 3 (BATF3) promotes CD8+ T-cell memory formation. This transcription factor regulates chromatin accessibility, enhancing CAR-T cell persistence for immunotherapy.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- CD8+ T lymphocytes transition from effector to memory cells post-antigen clearance.
- Sustained IL-2 production is a hallmark of functional cytotoxic T lymphocytes (CTLs).
Purpose of the Study:
- To identify transcription factors driving sustained IL-2 production in CTLs.
- To investigate the role of Basic Leucine Zipper ATF-Like Transcription Factor 3 (BATF3) in T-cell differentiation and memory formation.
Main Methods:
- Comparative analysis of influenza and cytomegalovirus-specific CTLs.
- Overexpression of BATF3 in virus-specific CTLs and CD19 chimeric antigen receptor T (CAR-T) cells.
- ATAC-seq analysis to assess chromatin accessibility changes.
Main Results:
- BATF3 overexpression enhanced proliferation in virus-specific CTLs and CAR-T cells.
- BATF3 facilitated the effector-to-memory transition, up-regulating memory genes and down-regulating exhaustion markers.
- ATAC-seq revealed BATF3 dynamically regulates chromatin accessibility impacting cytoskeletal organization, metabolism, and survival signaling.
Conclusions:
- BATF3 acts as a master regulator of CD8+ T-cell fate determination via chromatin remodeling.
- BATF3 offers a potential therapeutic target for improving CAR-T cell persistence in immunotherapy.
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