Modular delivery of co-stimulatory signals through a PD-1-based immunoswitch receptor improves the functionality of Hepatitis B Virus-specific engineered T cells - Scorecard - MDSpire

Modular delivery of co-stimulatory signals through a PD-1-based immunoswitch receptor improves the functionality of Hepatitis B Virus-specific engineered T cells

  • By

  • Luis Felipe Olguín-Contreras

  • Johanna Heep

  • Lisa Schiller

  • Eva Loffredo-Verde

  • Marvin M. Festag

  • Kai Metzger

  • Stephanie Färber

  • Merve Gültan

  • Margaret Tulessin

  • Susanne Wilde

  • Karin Wisskirchen

  • Elfriede Noessner

  • Ulrike Protzer

  • July 3, 2026

  • 0 min

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Clinical Scorecard: Enhanced Functionality of Engineered T Cells Targeting Hepatitis B Virus via Modular Co-Stimulatory Signal Delivery Using a PD-1 Immunoswitch Receptor

At a Glance

CategoryDetail
ConditionChronic Hepatitis B Virus Infection (cHBV)
Key MechanismsPD-1/PD-L1 interaction and engineered T-cell co-stimulation
Target PopulationIndividuals with chronic HBV infection
Care SettingAdoptive T-cell therapy

Key Highlights

  • PD-1-based immunoswitch receptors enhance T-cell functionality against HBV.
  • Modular delivery of co-stimulation improves T-cell activity in a tolerogenic liver environment.
  • PD-1_4-1BB demonstrates superior T-cell persistence and reduced exhaustion pathways.

Guideline-Based Recommendations

Diagnosis

  • Assess HBV infection status and liver function in patients.

Management

  • Consider engineered T-cell therapies for chronic HBV infection.

Monitoring & Follow-up

  • Monitor T-cell functionality and persistence in treated patients.

Risks

  • Evaluate potential for T-cell exhaustion and immune suppression.

Patient & Prescribing Data

Patients with chronic HBV infection requiring enhanced immune response.

Engineered T cells may provide a novel approach to overcome immune evasion by HBV.

Clinical Best Practices

  • Utilize PD-1-based immunoswitch receptors for targeted T-cell therapy.
  • Ensure proper spatial delivery of co-stimulatory signals in engineered T cells.

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