Collectively, we found that + 7 days B7H1/B7H3 serum levels can predict grade III-IV aGVHD, while only the + 7 days B7H1 serum level, together with viral infection and donor age, could independently predict GRM in patients with haplo-HSCT.
We conducted a multicenter, randomized study to assess the efficacy of using ex vivo cultured adult human MSC (remestemcel-L) in addition to second-line therapy to treat steroid-refractory aGVHD (NCT00366145).
We aim to analyze the association between NF-κB1 encoding p50 (rs28362491, -94 in.ertion/deletion ATTG) and miR-146a (rs2910164, G > C) polymorphisms and risk of aGVHD.
In the recipients of HID-SCT, the application of prophylactic DLI could reduce the risk of relapse, although with a higher incidence of DLI-associated acute GVHD than those of MSD-SCT.
Using major histocompatibility complex (MHC)-mismatched and MHC-matched murine BMT models, we found that Sirt-1<sup>-/-</sup> T cells had a reduced ability to induce acute GVHD (aGVHD) via enhanced p53 acetylation.
The increased serum Gas6 levels were also correlated with elevated lactate dehydrogenase, d-dimer, and plasmin inhibitor complex values in HSCT patients with aGVHD.
ECP therapy could significantly decrease CD56<sup>bri</sup>CD16<sup>-</sup> NK cells with shifting the quality from a cytotoxic to a regulatory pattern and additionally mature CD56<sup>dim</sup> NK cells via upregulation of CD57 in complete responding aGVHD patients.
We then present results of the two approaches to evaluate the potential of PTX3 as a prognostic marker of GvHD after haematopoietic stem cell transplantation.
We aim to analyze the association between NF-κB1 encoding p50 (rs28362491, -94 in.ertion/deletion ATTG) and miR-146a (rs2910164, G > C) polymorphisms and risk of aGVHD.
We aim to analyze the association between NF-κB1 encoding p50 (rs28362491, -94 in.ertion/deletion ATTG) and miR-146a (rs2910164, G > C) polymorphisms and risk of aGVHD.
We also performed single gene analyses of factors associated with tolerance (programmed death ligand-1 [PDL1], indoleamine 2,3 dioxygenase [IDO1], and T cell immunoreceptor with Ig and ITIM domains [TIGIT]) and found that significantly higher expression levels of these aGVHD inhibitory genes (PDL1, IDO1, TIGIT) at aGVHD onset became decreased in the steroid-refractory state.
In human umbilical vein endothelial cells (ECs), exogenous Gas6 or the exposure of sera isolated from patients with grade III aGVHD to ECs induced the downregulation of thrombomodulin and the upregulation of PAI-1, as well as the upregulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, which were inhibited by UNC2250, a selective Mer tyrosine kinase inhibitor.
Using major histocompatibility complex (MHC)-mismatched and MHC-matched murine BMT models, we found that Sirt-1<sup>-/-</sup> T cells had a reduced ability to induce acute GVHD (aGVHD) via enhanced p53 acetylation.
However, the 100-day cumulative incidences of grades II-IV and III-IV acute graft-versus-host disease (aGVHD) were lower in the FBA group [(8.93% versus 21.86%, P = 0.032) (1.79% versus 9.09%, P = 0.025)].
As the role of CD4<sup>+</sup>FoxP3<sup>+</sup> cells in the prevention of aGVHD is well established, we tested whether PSG1 has beneficial effects in a murine aGHVD transplantation model.
These findings reveal that Lkb1 downregulation contributes to multiple defects in Tregs in human aGVHD and highlight the Lkb1-related pathways that could serve as therapeutic targets that may potentially be manipulated to mitigate aGVHD.
We aim to analyze the association between NF-κB1 encoding p50 (rs28362491, -94 in.ertion/deletion ATTG) and miR-146a (rs2910164, G > C) polymorphisms and risk of aGVHD.
Here, we present the findings of a whole-body <sup>18</sup>FDG PET/CT with extensive and multifocal involvement of the GIT in a patient that developed severe acute GVHD 93 days post autologous SCT for Hodgkin's lymphoma.
On the other hand, Y-chromosome-encoded single-nucleotide polymorphisms in 4 genes (PCDH11Y, USP9Y, UTY, and NLGN4Y) did associate with acute GVHD in male patients with female donors.