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Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE247784 | GEO | 2026/04/08

REPOSITORIES: GEO

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Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection [ChIP-seq]

Project description:Splenic CD4+ T cells were sorted and stimulated with anti-CD3/CD28 antibodies in the presence of MAPK13 inhibitors or DMSO for 72h. And then cells were collected for ChIP-seq.

2026-04-08 | GSE247783 | GEO

Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection [RNA-seq]

Project description:Transcription factor phosphorylation is required for lymphocyte proliferation after activation. We here report an important role for MAPK13 in TCF-1 phosphorylation. Inhibition of MAPK13 results in decreased transcription of TCF-1 downstream genes and suppresses CD4+ lymphocyte proliferation and function.

2026-04-08 | GSE247781 | GEO

Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection

Project description:Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection

| PRJNA1040312 | ENA

Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection [RNA-seq]

Project description:Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection [RNA-seq]

| PRJNA1040309 | ENA

Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection [ChIP-seq]

Project description:Targeting one-carbon metabolism in stem cell-like T cells to prevent chronic graft rejection [ChIP-seq]

| PRJNA1040310 | ENA

Targeting the Mapk13-Tcf1-Slc7a5 Axis via One-Carbon Metabolic Regulation to Prevent Chronic Allograft Vasculopathy

Project description:Chronic allograft vasculopathy (CAV) is driven in part by stem-like Cd4⁺ T cells, but how these cells sustain their progenitor programs during chronic rejection remains unclear. Here, a metabolic-epigenetic axis is identified in which Mapk13 phosphorylates Tcf1 at T289, enabling Tcf1 to activate the amino acid transporter Slc7a5 and enhance methionine uptake. This rewires one-carbon metabolism and increases H3k4me3 enrichment at the Tcf7 locus, thereby maintaining stem-like Cd4⁺ T cells within rejecting grafts. Disruption of this circuit-via genetic deletion of Mapk13 or Slc7a5, or through dietary methionine restriction-reduces Tcf1⁺ Cd4⁺ T cell stemness and prevents CAV in mouse models. These findings reveal the Mapk13-Tcf1-Slc7a5 axis as a critical metabolic dependency of pathogenic T cells and highlight one-carbon metabolism as a promising target to promote long-term graft survival.

2026-04-08 | GSE314157 | GEO

Targeting one-carbon metabolism for cancer immunotherapy.

Project description:BackgroundOne-carbon (1C) metabolism is a metabolic network that plays essential roles in biological reactions. In 1C metabolism, a series of nutrients are used to fuel metabolic pathways, including nucleotide metabolism, amino acid metabolism, cellular redox defence and epigenetic maintenance. At present, 1C metabolism is considered the hallmark of cancer. The 1C units obtained from the metabolic pathways increase the proliferation rate of cancer cells. In addition, anticancer drugs, such as methotrexate, which target 1C metabolism, have long been used in the clinic. In terms of immunotherapy, 1C metabolism has been used to explore biomarkers connected with immunotherapy response and immune-related adverse events in patients.MethodsWe collected numerous literatures to explain the roles of one-carbon metabolism in cancer immunotherapy.ResultsIn this review, we focus on the important pathways in 1C metabolism and the function of 1C metabolism enzymes in cancer immunotherapy. Then, we summarise the inhibitors acting on 1C metabolism and their potential application on cancer immunotherapy. Finally, we provide a viewpoint and conclusion regarding the opportunities and challenges of targeting 1C metabolism for cancer immunotherapy in clinical practicability in the future.ConclusionTargeting one-carbon metabolism is useful for cancer immunotherapy.

| S-EPMC10819114 | biostudies-literature

Targeting IL-6 to prevent cardiac allograft rejection.

Project description:Outcomes following heart transplantation remain suboptimal with acute and chronic rejection being major contributors to poor long-term survival. IL-6 is increasingly recognized as a critical pro-inflammatory cytokine involved in allograft injury and has been shown to play a key role in regulating the inflammatory and alloimmune responses following heart transplantation. Therapies that inhibit IL-6 signaling have emerged as promising strategies to prevent allograft rejection. Here, we review experimental and pre-clinical evidence that supports the potential use of IL-6 signaling blockade to improve outcomes in heart transplant recipients.

| S-EPMC10191185 | biostudies-literature

Extracellular-acidosis restricts one-carbon metabolism and preserves T cell stemness

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-05 | GSE216623 | GEO

Targeting serine-glycine-one-carbon metabolism as a vulnerability in cancers.

Project description:The serine-glycine-one-carbon (SGOC) metabolic pathway is critical for DNA methylation, histone methylation, and redox homeostasis, in addition to protein, lipid, and nucleotide biosynthesis. The SGOC pathway is a crucial metabolic network in tumorigenesis, wherein the outputs are required for cell survival and proliferation and are particularly likely to be co-opted by aggressive cancers. SGOC metabolism provides an integration point in cell metabolism and is of crucial clinical significance. The mechanism of how this network is regulated is the key to understanding tumor heterogeneity and overcoming the potential mechanism of tumor recurrence. Herein, we review the role of SGOC metabolism in cancer by focusing on key enzymes with tumor-promoting functions and important products with physiological significance in tumorigenesis. In addition, we introduce the ways in which cancer cells acquire and use one-carbon unit, and discuss the recently clarified role of SGOC metabolic enzymes in tumorigenesis and development, as well as their relationship with cancer immunotherapy and ferroptosis. The targeting of SGOC metabolism may be a potential therapeutic strategy to improve clinical outcomes in cancers.

| S-EPMC10161514 | biostudies-literature

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