Project description:To identify kinases in immune cells of patients with SR-GVHD we isolated leukocytes and specifically enriched kinases via kinet-beads-technology. Rho Kinase Type 1 (ROCK1) was identified as the most abundant kinase in SR-GVHD.

2023-12-19 | PXD012036 | Pride

Rituximab for steroid-refractory chronic graft-versus-host disease.

Project description: Not available

| S-EPMC1895490 | biostudies-literature

Steroid Refractory Chronic Graft-Versus-Host Disease: Cost-Effectiveness Analysis.

Project description: Not available

| S-EPMC8058632 | biostudies-literature

Experimental Pharmaceuticals for Steroid-Refractory Acute Graft-versus-Host Disease.

Project description: Not available

| S-EPMC7705269 | biostudies-literature

Hedgehog blockade in steroid-refractory sclerotic chronic graft-versus-host disease.

Project description: Not available

| S-EPMC8511171 | biostudies-literature

Ruxolitinib in steroid refractory graft-vs.-host disease: a case report.

Project description: Not available

| S-EPMC4977623 | biostudies-literature

Immunopathology and biology-based treatment of steroid-refractory graft-versus-host disease.

Project description: Not available

| S-EPMC7378454 | biostudies-literature

Intestine epithelial Ceacam1 deficiency prevents steroid-refractory acute gut graft-versus-host disease

Project description:Steroid refractory gut acute graft-versus-host disease (SR-Gut-aGVHD) is the major cause of non-relapse death after allogeneic hematopoietic cell transplantation, due to poor understanding its pathogenesis. We recently reported that increase of donor-type IL-22+ T cells, IL-22-dependent dysbiosis, and loss of anti-inflammatory CX3CR1hi mononuclear phagocytes (MNP) play critical roles in SR-Gut-aGVHD pathogenesis, but the mechanisms remain unclear. Ceacam1 on intestinal epithelial cells (IECs) is proposed to regulate bacterial translocation and subsequent immune response in the gut tissues. Here, with imaging mass cytomtory (IMC), combined scRNA-Seq and ATAC-Seq, as well as high dimensional flow cytometry analysis, we show that Ceacam1 expression is enhanced on IECs in murine and human SR-Gut-aGVHD. Ceacam1 deficiency on host IECs effectively prevents SR-Gut-aGVHD in murine models. Ceacam1 deficiency on IECs results in 1) increase in frequencies of IL-22+IL-10+Foxp3+CD4+ peripheral Tregs (pTregs) while reducing conventional IL-22+CD4+ T (Tcon), Th/Tc1, and Th17 cells; 2) increase of beneficial commensal bacterial that augment colonic pTregs expansion, while reducing pathogenic bacteria and blocking E. Coli’s interaction with IECs; and 3) increase of anti-inflammatory CD103-CX3CR1hi MNP that produce IDO and IL-10, while reducing pro-inflammatory CD103+CX3CR1lo MNP that produce IL-6. Thus, specific targeting IEC Ceacam1 represents a novel approach for prevention of SR-Gut-aGVHD.

2026-05-28 | GSE268993 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data