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Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade
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Augmented CD47 expression impairs alloreactive T-cell clearance after allo-HCT.

Cindy Sheree Flamann1, Haroon Shaikh2, Carina Matos3

  • 1Department of Internal Medicine 5, Hematology and Oncology, University Hospital Erlangen, Erlangen, Germany.

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|May 7, 2025
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CD47 upregulation impairs T-cell clearance in Graft-versus-Host disease (GvHD) after transplantation. Targeting CD47 with antibodies or deficient cells enhances phagocytosis, reduces inflammation, and improves survival in GvHD.

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Area of Science:

  • Immunology
  • Transplantation Biology
  • Oncology

Background:

  • Graft-versus-Host disease (GvHD) is a major complication of allogeneic hematopoietic cell transplantation (allo-HCT).
  • Controlling inflammation is key to managing GvHD, with phagocytosis playing a role in resolving inflammation.
  • The specific role of phagocytosis in GvHD pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the role of the "don't eat me" signal CD47 in GvHD.
  • To explore CD47 as a therapeutic target for eradicating alloreactive T-cells post-allo-HCT.
  • To assess the impact of modulating CD47 on T-cell phagocytosis and GvHD outcomes.

Main Methods:

  • Analysis of global datasets to assess CD47 expression on T-cells in inflamed tissues.
  • Examination of CD47 levels in the gastrointestinal tract (GIT) of GvHD patients and mice post-allo-HCT.
  • In vitro studies using anti-CD47 antibodies to assess antibody-dependent cellular phagocytosis (ADCP) of T-cells.
  • In vivo studies administering anti-CD47 antibodies or CD47-deficient T-cells to GvHD mouse models.

Main Results:

  • CD47 expression is significantly upregulated on T-cells in the inflamed ileum of GvHD patients and mice.
  • Activated donor T-cells suppress ADCP via CD47 signaling, leading to impaired phagocytosis.
  • Treatment with anti-CD47 antibodies restored ADCP, enhanced T-cell phagocytosis in the GIT, and improved survival in mice.
  • Transplantation of CD47-deficient donor T-cells improved clinical GvHD scores and survival.

Conclusions:

  • CD47 upregulation is a critical mechanism in GvHD, causing impaired phagocytic clearance of alloreactive T-cells.
  • Targeting CD47 with antibodies represents a promising therapeutic strategy to enhance phagocytosis of alloreactive T-cells.
  • Anti-CD47 therapy could facilitate inflammation resolution and improve outcomes after allo-HCT.