Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we investigated the impact of differential dosing and timing of PTCy on its efficacy in preventing GVHD in a murine MHC-haploidentical HCT model.
|
31586477 |
2020 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, we prove a role for microglia in CNS-GVHD, identify the TAK1/TNF/MHC-II axis as mediator of CNS-GVHD and provide a novel TAK1 inhibitor-based approach against GVHD-induced neurotoxicity.
|
31846439 |
2020 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
As for each HLA locus, HLA-A mismatch correlated with decreased rate of platelet engraftment (HR 0.740, P = .003); HLA-B mismatch independently correlated with decreased relapse rate (HR 0.494, P = .032) and improved disease-free survival and overall survival (HR 0.514, P = .003; HR 0.494, P = .002, respectively); HLA-C mismatch appeared to be protective for transplant-related mortality (TRM) (HR 0.567, P = .039); HLA-DRB1 mismatch was associated with increased cumulative incidence of grade II-IV acute graft-vs.-host disease (GVHD) (HR 1.942, P = .002).
|
29335631 |
2018 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Notably, transplant of extremely low numbers of these Tregs (1:6 expanded Tregs/conventional T cells) suppressed GVHD after an MHC-mismatched aHSCT.
|
29751114 |
2018 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
A significant RR of HLA allele mismatch compared with match was seen with HLA-A, -B, -C, and -DPB1 for grade III-IV acute graft-versus-host disease (GVHD), and HLA-C for chronic GVHD.
|
25519752 |
2015 |
Graft-vs-Host Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The risk of GvHD furthermore increased when recipients heterozygous for HLA-C KIR ligand groups (C1/C2) were transplanted from donors completely lacking activating KIRs (HR 6.1, 95% CI 1.9-19.2, P = 0.002).
|
22077388 |
2012 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Similarly, in an MHC-mismatched system, T(EM) cells with a proven increased precursor frequency of alloreactive clones only caused limited GVHD.
|
21660940 |
2011 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
HLA-Cw disparity in a donor increases the risk of acute graft-vs-host disease (GVHD) after bone marrow transplantation.Acute GVHD is mediated by donor CTLs.
|
19812210 |
2009 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
In MHC-mismatched mouse models, these contacts were not required for GVHD.
|
18223170 |
2008 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
We previously showed that engraftment of MHC-mismatched BM is enhanced and GVHD abrogated in recipients homozygous for a germline SHIP mutation.
|
17312133 |
2007 |
Graft-vs-Host Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Despite contemporary typing procedures for bone marrow transplantation (BMT), graft-versus-host disease (GVHD) continues to be a major complication of transplants performed between MHC-matched donors and recipients.
|
10382959 |
1999 |
Graft-vs-Host Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Multivariate analysis showed that incompatibility for HLA-A alleles and incompatibility for HLA-C alleles were independent risk factors for severe acute graft-versus-host disease (GVHD) (HLA-A, P=0.006; HLA-C, P=0.001).
|
9780337 |
1998 |