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| Open AccessROCK1/2 signaling contributes to corticosteroid-refractory acute graft-versus-host disease
Steroid-refractory acute graft-versus-host disease (aGVHD) is associated with a low one-year survival rate. Here, the authors show that ROCK1 is upregulated in leukocytes from patients with steroid-refractory aGVHD and that ROCK1/2 inhibition reduces the severity of aGVHD in mice by interfering with activation of multiple immune cell types.
- Kristina Maas-Bauer
- , Anna-Verena Stell
- & Robert Zeiser
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Article
| Open AccessData-driven grading of acute graft-versus-host disease
Acute GVHD severity grading is based on target organ assessments. Here, the authors show that data-driven grading can identify 12 distinct grades with specific aGVHD phenotypes, which are associated with clinical outcomes, and that their method outperformed conventional gradings.
- Evren Bayraktar
- , Theresa Graf
- & Amin T. Turki
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| Open AccessClonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy
Immune checkpoint inhibitors (ICI) may have unanticipated side effects in transplant recipients who subsequently develop tumors. Here the authors used single-cell sequencing to identify and characterize allogeneic reactive T cells that developed after an ICI course for melanoma in a transplant recipient.
- Garrett S. Dunlap
- , Daniel DiToro
- & Deepak A. Rao
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| Open AccessSingle-cell transcriptomic analysis reveals disparate effector differentiation pathways in human Treg compartment
Human Treg cells are central to immune tolerance, yet their heterogeneity and differentiation remain incompletely understood. Here the authors perform single-cell RNA and T cell receptor sequencing to resolve Treg cells from healthy individuals and patients with or without acute graft-versus-host disease revealing Treg complexity in health and disease.
- Yuechen Luo
- , Changlu Xu
- & Xiaoming Feng
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Article
| Open AccessIL-22-dependent dysbiosis and mononuclear phagocyte depletion contribute to steroid-resistant gut graft-versus-host disease in mice
Pathogenesis of steroid-resistant gut acute graft-versus-host-disease (SR-Gut-aGVHD) remains unclear., Here the authors show in mouse models that dysbiosis caused by the expansion of Th/Tc22, as well as depletion of CX3CR1hi mononuclear phagocytes resulted from the reduction of Th/Tc1, contributes to SR-Gut-aGVHD onset.
- Qingxiao Song
- , Xiaoning Wang
- & Defu Zeng
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Article
| Open AccessLongitudinal dynamics of gut bacteriome, mycobiome and virome after fecal microbiota transplantation in graft-versus-host disease
Fecal microbiota transplant (FMT) is emerging as a potential treatment for graft-versus-host disease (GvHD). Here, the authors examine temporal dynamics of the bacteriome, mycobiome, and virome of a patient with GvHD who received multiple FMTs.
- Fen Zhang
- , Tao Zuo
- & Siew C. Ng
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Article
| Open AccessSomatic mTOR mutation in clonally expanded T lymphocytes associated with chronic graft versus host disease
Chronic graft versus host disease (cGvHD) is a major cause of morbidity and mortality in allogeneic bone marrow transplantation. Here the authors identify a recurrent activating mTOR mutation in expanded donor T-cell clones of 3 cGvHD patients, which suggests somatic mutations may contribute to GvHD pathogenesis and opens avenues to targeted therapies.
- Daehong Kim
- , Giljun Park
- & Satu Mustjoki
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| Open AccessMicrobial metabolite sensor GPR43 controls severity of experimental GVHD
The microbial metabolite sensor GPR43 has been previously shown to be a crucial modulator of immune responses. Here the authors show GPR43 is required for controlling disease pathology severity in the context of experimental models of GVHD.
- Hideaki Fujiwara
- , Melissa D. Docampo
- & Pavan Reddy
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Article
| Open AccessActivated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells
Graft-vs.-host disease is a complication of allogenic hematopoietic stem cell transplantation, and is associated with endothelial dysfunction. Here the authors show that activated protein C signals via PAR2/PAR3 to expand Treg cells, mitigating the disease in mice.
- Satish Ranjan
- , Alexander Goihl
- & Berend Isermann