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MEK inhibition prevents human skin graft rejection by promoting CD8+TCF1+ T cells over CD8 effector differentiated T cells.

ABSTRACT: MEK inhibition prevents human skin graft rejection by promoting CD8+TCF1+ T cells over CD8 effector differentiated T cells.

PROVIDER: PRJNA1107267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28878769_1.fastq.gz	Fastqsanger.gz
	SRR28878769_2.fastq.gz	Fastqsanger.gz
	SRR28878770_1.fastq.gz	Fastqsanger.gz
	SRR28878770_2.fastq.gz	Fastqsanger.gz
	SRR28878771_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

MEK inhibition prevents human skin graft rejection by promoting CD8+TCF1+ T cells over CD8 effector differentiated T cells.

Project description:While graft loss remains primarily attributed to rejection, the adverse effects of immunosuppressive therapies significantly contribute to patient morbidity and mortality. Therefore, it is imperative to develop treatments that both prevent alloimmune damage to the transplant and are well tolerated. MEK inhibition has recently been showed to be effective in controlling the alloimmune response in experimental mouse graft-versus-host disease, without abrogating anti-tumor nor anti-viral immunity. Here, we demonstrate that pharmacological MEK inhibition delays human skin graft rejection by human T cells in a preclinical humanized mouse model. Although similar graft infiltration was observed between treated and untreated animals, human epidermal cells were protected by the treatment. Single cell RNAseq analysis of the spleen immune cells revealed that MEK inhibition treatment inhibits CD8 T cell development to an effector phenotype and promotes the accumulation of CD8+TCF1+ stem-like cells. Furthermore, analysis of the CD4 cells showed that MEK inhibition improved CD4 T cell recovery by preserving IL7R expression on CD4 T cells and favored CD4 T cells engagement in the Th1 lineage rather than the Tfh lineage. These findings suggest that MEK inhibition could be an innovative approach to combining allogeneic immune response control and tissue protection after transplantation.

2025-05-01 | GSE266482 | GEO

Impact of Tcf1 and Lef1 deficiency on histone marks and Tcf1 binding in CD8 T cells

Project description:Comparison of epigenome and Tcf1 occupancy between control and Tcf1/Lef1-deficient CD8 T cells Control mice or those are deficient for Tcf1 and Lef1 transcription factors (deleted by CD4-Cre) were used to isolate thymocytes. The thymocytes were surface-stained to identify TCRbeta high, CD69â, CD24â CD8+ subsets. These cells were sorted for ChIPseq analysis of various histone marks. Control mice or those are deficient for Tcf1 (deleted by CD4-Cre) were used to isolate thymocytes. The splenocytes were surface-stained to identify TCRbeta high, CD8+ subsets. These cells were sorted for ChIPseq analysis of Tcf1 binding locations.

2016-02-12 | E-GEOD-73239 | biostudies-arrayexpress

Analysis of allospecific CD8 T cells in murine pregnancy or graft rejection

Project description:Analysis of allospecific CD8 T cells in murine pregnancy or graft rejection

| PRJNA892954 | ENA

Genome-wide maps of Tcf1 binding locations in splenic CD8 T cells.

Project description:We mapped genome-wide Tcf1 binding locations in mature CD8 T cells to identify its direct target genes. This experiment aims to identify genome-wide binding locations for Tcf1 transcription factor in mature CD8 T cells. The CD8 T cells were isolated from wild-type C57BL/6 mice by negative selection. The chromatin fragments were immunoprecipitated by an anti-Tcf1 antiserum or control rabbit serum (without immunization). The immunoprecipitated fragments were then used in high throughput sequencing. Data processing then revealed >3000 high-confidence Tcf1 binding peaks across the CD8 T cell genome. One important finding is that Tcf1 binds directly to Cd4 gene silencer, and thus explain its important role in suppressing the CD4 coreceptor in mature CD8 T cells.

2014-03-05 | E-GEOD-52070 | biostudies-arrayexpress

Analysis of graft-infiltrating CD8+ T cell profile after CD3 antibody therapy

Project description:We performed a global gene expression analysis comparing intragraft tolerant CD8+ T cells from CD3 antibody-treated mice showing permanent islet graft survival to intra-graft effector CD8+ T cells isolated from untreated mice showing acute rejection of islet allografts. The objective was to emphasize the anergic profile of CD8+ T cells residing within the pancreatic islet allograft of mice rendered tolerant following CD3 antibody therapy.

2017-02-10 | GSE68208 | GEO

Impact of Tcf1 and Lef1 deficiency on mature CD8 thymocytes

Project description:Comparison of transcriptome between control and Tcf1/Lef1-deficient mature CD8 thymocytes Control mice or those are deficient for Tcf1 and Lef1 transcription factors (deleted by CD4-Cre) were used to isolate thymocytes. The thymocytes were surface-stained to identify TCRbeta high, CD69â, CD24â CD8+ subsets. These cells were sorted for RNAseq analysis.

2016-02-12 | E-GEOD-73238 | biostudies-arrayexpress

Transcriptome analysis of allospecific CD8 T cells in murine pregnancy or graft rejection

Project description:Transcriptome analysis of allospecific CD8 T cells in murine pregnancy or graft rejection

| PRJNA892958 | ENA

Epigenetic analysis of allospecific CD8 T cells in murine pregnancy or graft rejection

Project description:Epigenetic analysis of allospecific CD8 T cells in murine pregnancy or graft rejection

| PRJNA892087 | ENA

Defining TCF1+ progenitor allogeneic CD8 T cell subset in acute graft-versus-host disease

Project description:Defining TCF1+ progenitor allogeneic CD8 T cell subset in acute graft-versus-host disease

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Leukocyte accumulation in graft blood vessels during self-limiting acute rejection of rat kidneys Immunobiology

Project description:Acute rejection episodes trigger chronic renal allograft vasculopathy. Numerous leukocytes, predominantly monocytes, accumulate in graft blood vessels during reversible acute rejection preceding chronic rejection of rat kidneys. We speculate that they contribute to transplant vasculopathy and set out to characterize them. Allogeneic renal transplantation was performed in the Fischer 344 to Lewis rat strain combination, Lewis isografts served as controls. Leukocytes were harvested by intensive perfusion of graft blood vessels and subjected to flow cytometry, quantitative RT-PCR and genome-wide transcriptional profiling. Kidneys of LEW and F344 rats were transplanted in LEW rats. Five biological replicates were performed for both isogenic and allogenic transplantation. Transcriptomes of allogenics were compared to isogenics on 5 dual-color hybridizations.

2010-09-24 | E-GEOD-18266 | biostudies-arrayexpress

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