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Tumor Immunotherapy01:27

Tumor Immunotherapy

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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  11. Low-strength Type I Interferon Signaling Promotes Car T-cell Treatment Efficacy

Low-Strength Type I Interferon Signaling Promotes CAR T-Cell Treatment Efficacy

Erting Tang1, Yifei Hu1,2, Guoshuai Cao1

  • 1Pritzker School of Molecular Engineering, University of Chicago, Chicago, IL 60637, USA.

Biorxiv : the Preprint Server for Biology
|June 4, 2025

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High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
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View abstract on PubMed

Summary
This summary is machine-generated.

Type I interferon (IFN-I) signaling enhances chimeric antigen receptor (CAR) T-cell therapy for relapsed/refractory diffuse large B-cell lymphoma (r/r DLBCL). Low-strength IFN-I signaling improved CAR T-cell efficacy, while high-strength signaling reduced it.

Area of Science:

  • Immunology
  • Oncology
  • Cell Therapy

Background:

  • Chimeric antigen receptor (CAR) T-cell therapy, specifically CD19-directed CAR T-cell therapy, has shown promise for relapsed/refractory diffuse large B-cell lymphoma (r/r DLBCL).
  • However, a significant proportion of patients (up to 60%) do not achieve a complete response, necessitating strategies to improve therapeutic efficacy.

Purpose of the Study:

  • To identify molecular determinants of response to axicabtagene ciloleucel in r/r DLBCL patients.
  • To develop a novel strategy to enhance CAR T-cell therapy efficacy by modulating type I interferon (IFN-I) signaling during ex vivo manufacturing.

Main Methods:

  • Single-cell transcriptomics analysis of CAR T-cell infusion products from eight r/r DLBCL patients with varying clinical responses.
  • Ex vivo incorporation of low-strength and high-strength IFN-I signaling during the manufacturing of CD28- and 4-1BB-costimulated CAR T-cells.
Keywords:
axicabtagene ciloleucel (axi-cel)chimeric antigen receptor (CAR)diffuse large B-cell lymphoma (DLBCL)lisocabtagene maraleucel (liso-cel)

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  • Assessment of CAR T-cell cytotoxicity and in vivo efficacy in preclinical models.

    • Main Results:

    • Infusion products from complete responders exhibited enriched type I interferon (IFN-I) signaling signatures compared to those with progressive disease.
    • Low-strength IFN-I signaling enhanced CAR T-cell cytotoxicity and in vivo efficacy for both CD28- and 4-1BB-based CAR constructs.
    • High-strength IFN-I signaling impaired CAR T-cell viability and in vivo efficacy.

    Conclusions:

    • Type I interferon (IFN-I) is a potent, costimulation-independent enhancer of CAR T-cell efficacy.
    • Incorporating low-strength IFN-I signaling during ex vivo manufacturing represents a translationally feasible approach to improve CAR T-cell therapies for r/r DLBCL.
    • This strategy leverages an FDA-approved agent and is compatible with existing CAR T-cell manufacturing processes.
    type I interferon (IFN-I)