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Acute graft-versus-host disease does not require alloantigen expression on host epithelium
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Regenerating islet-derived 3-alpha is a biomarker of gastrointestinal graft-versus-host disease.
REG3α is a plasma biomarker of GI GVHD that can be combined with clinical stage and histologic grade to improve risk stratification of patients and correlated most closely with lower GI GvHD.
Donor-derived thymic-dependent T cells cause chronic graft-versus-host disease.
It is demonstrated for the first time that T cells that escape from negative thymic selection could cause chronic GVHD after allogeneic BMT, and it is suggested that self-reactivity of donor T cells plays a role in this chronicGVHD, and improvement in theThymic function may have a potential to decrease chronic GvHD.
LPS antagonism reduces graft-versus-host disease and preserves graft-versus-leukemia activity after experimental bone marrow transplantation.
Findings reveal a critical role for LPS in the early inflammatory events contributing to GVHD and suggest that a new class of pharmacologic agents, LPS antagonists, may help to prevent GV HD while preserving T cell responses to host antigens and GVL activity.
Immune signature drives leukemia escape and relapse after hematopoietic cell transplantation
The results demonstrate that the deregulation of pathways involved in T cell-mediated allorecognition is a distinctive feature and driver of AML relapses after allo-HCT, which can be rapidly translated into personalized therapies.
The Pathophysiology of Acute Graft-versus-Host Disease
The pathophysiology of acute graft-versus-host disease (GVHD) is a complex process that can be conceptualized in three phases; donor T-cells recognize alloantigens on host APCs, and target cells undergo apoptosis mediated by cellular effectors and inflammatory cytokines such as TNF-α.
Microbiota as Predictor of Mortality in Allogeneic Hematopoietic-Cell Transplantation.
BACKGROUND Relationships between microbiota composition and clinical outcomes after allogeneic hematopoietic-cell transplantation have been described in single-center studies. Geographic variations
Host Dendritic Cells Alone Are Sufficient to Initiate Acute Graft-versus-Host Disease1
It is demonstrated that host-derived DCs are critical in priming donor CD4+ and CD8+ T cells to cause GVHD, and selective targeting of host DCs may be a promising strategy to prevent GV HD.
Enhanced allostimulatory activity of host antigen-presenting cells in old mice intensifies acute graft-versus-host disease.
A hitherto unsuspected mechanism of amplified donor T cell responses by aged allogeneic host APCs that increases acute GVHD in aged recipients in this BMT model is demonstrated.