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December 8, 2025BloodOpen Access

Monocarboxylate transporter 1 deficient donor T cells rewire metabolism and ameliorate aGVHD lethality

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Authors

ASAsim SahaCMCameron McDonald-HymanJRJeffrey C. Rathmell

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Overview

MCT1 knockout alters metabolism and enhances survival in aGVHD, suggesting potential therapeutic strategies for transplant recipients.

Key Points

  • MCT1 deletion significantly reduced T cell proliferation by up to 30%, improving survival rates in aGVHD models.
  • Observations revealed altered metabolic profiles, showing diminished lactate and enhanced glucose-derived metabolites in MCT1 knockout T cells.
  • Analysis of bone marrow transplants highlighted that MCT1 KO T cells attenuated cytotoxicity while increasing regulatory T cell populations.
  • Targeting MCT1 could provide a novel therapeutic strategy in aGVHD treatment while preserving graft-versus-tumor effects.

Cite This Study

Saha et al. (2025) studied this question.

synapsesocial.com/papers/69362f484fa91c937236d6e4https://doi.org/10.1182/blood-2025-5867
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Also Consider

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

  1. 1Ornithine 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 manner2025
  2. 2IFNγ-driven MHC class II expression by intestinal epithelial cells dictates local cytolytic Th1 cell differentiation and intestinal stem cell loss2025
  3. 3In Vivo clonal dynamics of alloreactive CAR T cells reveal mechanisms limiting gvhd risk following allogeneic CAR T cell therapy2025
  4. 4Acetyl-CoA carboxylase 1 inhibition increases Treg metabolism and graft-versus-host disease treatment efficacy via mitochondrial fusion2025 · 9 citations
  5. 5Overexpression of CD103 on regulatory T cells mitigates acute graft-versus-host disease via promotion of tolerogenic dendritic cell networks2025 · 1 citations