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Transplant anti-host disease (GvHD) is a major obstacle to hematopoietic stem cell transplantation (AHSCT).
a clear diagnosis of graft anti-host disease requires invasive testing and biopsies of the tissue under examination, but there is a higher risk of bleeding and infection.
T cells are at the heart of the pathogenesis of GvHD, and studies in mouse models of chronic GvHD have shown that CD4-T cells with iso-reactive organisms enter the target organ before obvious symptoms appear.
Given that increased glycolysis is an early feature of T-cell activation, Assmann and others speculate that in vivo glycolysis metabolic imaging can detect liver GvHD invasively, as GvHD occurs when activated CD4-T cells enter.
Has been experimentally proven that ultrapolar 13C-acetone acid MRI can detect an increase in acetone-lactic acid conversion in the liver before symptoms occur in animals, but this is not the same during cGvHD, which is followed by significant symptoms.
same time, the analysis of transcriptional groups, proteins, metabolites and in-body metabolic activity confirmed that CD4-T-effect memory cells (the main pathogenic CD4-T-cell subgroups) have high glycolysis.
preliminary data on single-cell sequencing of circulating T-cells in patients treated with the allogeneic HSCT also suggest that increased glycolysis may be a feature of early GvHD.
, metabolic imaging is increasingly used in clinical practice and may contribute to the non-invasive early detection of GvHD after AHSCT.
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