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December 8, 2025BloodOpen Access

Ornithine decarboxylase deficiency in donor T cells preserves strong GVL activity while attenuating acute and preventing steroid-resistant gut GVHD in a recipient tissue PD-L1-dependent manner

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Authors

MZMoqian ZhengXWXiwei WuRNRyotaro Nakamura

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Overview

Observational analysis revealed that ornithine decarboxylase deficiency lowers graft-vers-host disease severity in recipients, suggesting a therapeutic advantage for GVL effects.

Key Points

  • GVH activity preserved with ornithine decarboxylase deficiency, enabling significant graft-vers-host disease reduction.
  • Dexamethasone treatment in this context reduced graft-vers-host disease while maintaining GVL activity.
  • Analysis using a murine Allo-HCT model demonstrated enhanced reactive oxygen species levels associated with T cell exhaustion.
  • Identifying metabolic pathways could lead to novel strategies in managing graft-vers-host disease and improving GVL outcomes.

Cite This Study

Zheng et al. (2025) studied this question.

synapsesocial.com/papers/69362f744fa91c937236e28ahttps://doi.org/10.1182/blood-2025-5868
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Monocarboxylate transporter 1 deficient donor T cells rewire metabolism and ameliorate aGVHD lethality2025
  2. 2Galectin-3 in host murine models lessens the severity of graft-versus-host disease by preserving intestinal stem cells irrespective of gut microbiota composition2025
  3. 3GLP-1R signaling does not modify the severity of experimental graft versus host disease2025 · 4 citations
  4. 4Thymic dysfunction promotes the emergence of pathogenic peripheral CD4⁺CD8⁺ T cells and induces tissue injury in acute gvhd2025
  5. 5Longitudinal multiproteomic analysis reveals persistent underlying inflammation in acute graft-versus-host disease patients responding to corticosteroid treatment2025