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Investigating Target Gene Function in a CD40 Agonistic Antibody-induced Colitis Model using CRISPR/Cas9-based Technologies
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EBAG9 silencing exerts an immune checkpoint function without aggravating adverse effects.

Anthea Wirges1, Mario Bunse2, Jara J Joedicke1

  • 1Translational Tumorimmunology, Max-Delbrück-Center for Molecular Medicine, 13125 Berlin, Germany.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|July 13, 2022
PubMed
Summary

Silencing estrogen receptor-binding fragment-associated antigen 9 (EBAG9) in engineered T cells enhances their tumor-killing ability. This approach improves adoptive T cell therapy efficacy and reduces the required therapeutic dose without compromising safety.

Keywords:
adoptive T cell therapycancer immunotherapychimeric antigen receptor T cellscytolytic capacityhematologic malignanciesleukemiamultiple myelomasecretory pathway

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Area of Science:

  • Immunology
  • Cell Biology
  • Cancer Therapy

Background:

  • Chimeric antigen receptor (CAR) T cells have transformed B cell malignancy treatment.
  • Enhancing CAR T cell efficacy and safety remains a critical challenge.
  • Estrogen receptor-binding fragment-associated antigen 9 (EBAG9) inhibits cytotoxic T lymphocyte enzyme release.

Purpose of the Study:

  • To investigate the potential of EBAG9 silencing to improve adoptive T cell therapy.
  • To assess the impact of EBAG9 downregulation on T cell effector function and safety.
  • To evaluate EBAG9's role as an immune checkpoint.

Main Methods:

  • MicroRNA (miRNA)-mediated EBAG9 downregulation in CD8+ T cells (CTLs).
  • Tumor models in mice and xenotransplantation models with human CAR T cells.
  • Transcriptome profiling to assess genotoxicity and differentiation.
  • Retrovirus transduction to link CAR/TCR expression with EBAG9 silencing.

Main Results:

  • EBAG9 silencing in CTLs improved cytolytic competence against tumors.
  • EBAG9 deletion converted a minor histocompatibility antigen into a rejection antigen.
  • Fewer EBAG9-silenced human CAR T cells controlled tumor growth in xenografts.
  • Transcriptome analysis showed no increased risks of genotoxicity or aberrant differentiation.
  • Cytokine release syndrome-associated cytokines were unaffected despite enhanced efficacy.

Conclusions:

  • EBAG9 silencing enhances the effector capacity of TCR- and CAR-engineered T cells.
  • This strategy improves tumor eradication, simplifies manufacturing, and reduces therapeutic dosage.
  • EBAG9 silencing represents a promising approach for enhancing adoptive T cell therapy.