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Blunting specific T-dependent antibody responses with engineered "decoy" B cells.

Ragan A Pitner1, Jaime L Chao2, Noelle P Dahl3

  • 1Department of Immunology, University of Washington School of Medicine, Seattle, WA 98109, USA; Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA 98101, USA.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|August 28, 2024
PubMed
Summary

Engineered B cells can suppress harmful antibody responses in genetic disorders. This novel cell therapy approach reduces specific antibody production, offering a potential new treatment for protein deficiency diseases.

Keywords:
B cell engineeringBlimp1CRISPRantibodyantibody inhibitorscell therapygene therapygerminal centershemophiliaimmune tolerance

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Area of Science:

  • Immunology
  • Cell Therapy
  • Genetic Engineering

Background:

  • Antibody inhibitors complicate treatments for inherited protein deficiencies, reducing the effectiveness of protein replacement and gene therapies.
  • B cells possess unique antigen recognition and presentation capabilities, making them potential candidates for cell-based therapies.

Purpose of the Study:

  • To investigate the therapeutic potential of ex vivo antigen-primed Blimp1-knockout "decoy" B cells in downregulating host antigen-specific humoral responses.
  • To assess the efficacy of decoy B cells in mitigating antibody production in a mouse model of factor VIII deficiency.

Main Methods:

  • CRISPR-Cas9 gene editing was used to create Blimp1-knockout B cells incapable of plasma cell differentiation.
  • Antigen-specific B cells were primed ex vivo and adoptively transferred into recipient mice.
  • Mice were immunized with conjugated antigens, and humoral responses, including IgG production and functional inhibition, were measured.

Main Results:

  • Adoptively transferred decoy B cells were efficiently recruited into germinal centers, outcompeting endogenous B cells.
  • Decoy B cells dose-dependently suppressed antigen-specific IgG responses without affecting unrelated antibody production.
  • Treatment with antigen-pulsed decoy B cells in factor VIII-knockout mice significantly reduced FVIII-specific IgG production and functional inhibition.

Conclusions:

  • Ex vivo antigen-primed decoy B cells can effectively suppress antigen-specific humoral immunity.
  • This approach shows therapeutic promise for managing antibody inhibitor issues in inherited protein deficiency disorders.
  • Decoy B cell therapy offers a targeted strategy to blunt specific antibody responses while preserving overall immune function.