The aims of the current study were to investigate: (1) red blood cell (RBC) engraftment and (2) EC chimerism as a potential result of replacement of recipient EC by donor bone marrow (BM)-derived EC in a patient following major ABO-incompatible (A to O) and gender-mismatched HSCT, who died at day 350 of severe acute GVHD.
Altogether, our findings support that the allogeneic immune response during acute GvHD might be influenced by bile acids and by the decreased production of AhR ligands by microbiota that could limit indoleamine 2,3-dioxygenase induction and influence allogeneic T cell reactivity.
We examined genes triggered by microbial ligands to stimulate gut repair, amphiregulin (AREG) and the aryl hydrocarbon receptor (AhR), and found that both AREG and AhR gene expression levels were increased at aGVHD onset and remained elevated in steroid-refractory aGVHD.
Two-year OS was significantly better in patients with SR aGVHD with a serum albumin ≥35 g/l compared to SR with albumin <35 g/l [70% (95% CI = 64-76%) vs. 49% (95% CI = 42-56%), P < 0·0001].
Patient factors (age, sex, underlying diseases, hemoglobin, serum albumin, and Karnofsky performance status score before transplant) and transplant factors (conditioning regimen, days to neutrophil engraftment, grades of acute graft-versus-host disease [GVHD], infections, and the interval between pre- and post-evaluation) were collected via chart review, and were used for correlational and comparison analyses in order to identify the variables associated with reduced post-HSCT leg extension torque and peak VO<sub>2</sub>.
Simvastatin improved the survival of aGVHD mice, attenuated the histopathological GVHD grades and plasma levels of Ang-2, and elevated the plasma levels of Ang-1 as well as the aortic endothelial levels of Ang-1 and Ang-2.
In this study, we explored changes in Angiopoietin-1 (Ang-1) and Ang-2 expression in a aGVHD mouse model and determined whether simvastatin prevents GVHD through regulating Ang-1 and Ang-2 expression.
Our data mechanistically link APC-derived complement to T cell-mediated GvHD and support complement inhibition as a therapeutic strategy for GvHD in humans.
We examined genes triggered by microbial ligands to stimulate gut repair, amphiregulin (AREG) and the aryl hydrocarbon receptor (AhR), and found that both AREG and AhR gene expression levels were increased at aGVHD onset and remained elevated in steroid-refractory aGVHD.
Recipient mismatching for the minor histocompatibility antigen HA-1 has been associated with acute graft-versus-host disease after allogeneic marrow transplantation.
Correlation between disparity for the minor histocompatibility antigen HA-1 and the development of acute graft-versus-host disease after allogeneic marrow 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.
Because of almost absolute linkage disequilibrium observed among all 5 SNPs, association of 2 major ATM haplotypes (ATM1/ATM2) with RR-GIT and acute GVHD (aGVHD) was analyzed.
Our NOD/SCID-beta2m(null) mouse model provides a system to study the pathophysiology of acute GVHD induced by human T cells and aids in development of more effective therapies for human GVHD.
We created humanised mice model for chronic GVHD (cGVHD) by injecting cord blood (CB)-derived human CD34<sup>+</sup>CD38<sup>-</sup>CD45RA<sup>-</sup> haematopoietic stem/progenitor cells (HSPCs) into hIL-6 transgenic NOD/SCID/Il2rgKO (NSG) newborns, and compared GVHD progression with NSG newborns receiving CB CD34<sup>-</sup> cells mimicking acute GVHD.
These data provide a comprehensive elucidation of the T cell transcriptome in primate acute GVHD and suggest that AURKA should be considered a target for preventing GVHD, which, given the many available AURKA inhibitors in clinical development, could be quickly deployed for the prevention of GVHD.
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.