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Effect of Tigit deficiency on CD4 T cell

ABSTRACT: Effect of Tigit deficiency on CD4 T cell

PROVIDER: PRJNA1147618 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30220829_1.fastq.gz	Fastqsanger.gz
	SRR30220829_2.fastq.gz	Fastqsanger.gz
	SRR30220830_1.fastq.gz	Fastqsanger.gz
	SRR30220830_2.fastq.gz	Fastqsanger.gz
	SRR30220831_1.fastq.gz	Fastqsanger.gz

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Effect of Tigit deficiency on CD4 T cell

Project description:To investigate the role of TIGIT in CD4+ T cell differentiation, Total CD4+ T cells were isolated from WT or Tigit -/- mice. Cells were stimulated with anti-CD3/CD28 for 3 d. Cells were then collected and total RNA was extracted.

2025-03-26 | GSE274668 | GEO

The Co-inhibitory Receptor TIGIT has T cell intrinsic functions

Project description:We compared the gene expression in wild type CD4+ T cells stimulated with agonistic anti-TIGIT 4D4 antibody to that of isotype and TIGIT-deficient (KO) controls.

2011-01-01 | E-MEXP-2847 | biostudies-arrayexpress

TIGIT+ Tregs

Project description:TIGIT+ Tregs suppress Th1 and Th17 responses while sparing Th2 responses. Analysis of global gene expression of TIGIT+ vs. TIGIT- Tregs from naive mice reveled that TIGIT+ Tregs display an activated phenotype and are enriched for Treg signature genes including the Treg effector molecule Fgl2 which enables them to selectively spare Th2 responses. TIGIT+ and TIGIT- Tregs were sorted from naïve Foxp3-GFP KI mice (pooled spleen and lymph nodes) TIGIT: T cell immunoreceptor with Ig and ITIM domains

2014-12-12 | E-GEOD-56299 | biostudies-arrayexpress

Effect of Foxo1 deficiency in naive CD4 T cell activation in vitro

Project description:Effect of Foxo1 deficiency in naive CD4 T cell activation in vitro

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The immune checkpoint TIGIT is upregulated on T cells during bacterial infection and is a potential target for immunotherapy

Project description:Antibiotic resistance is a major public health threat, and alternatives to antibiotic therapy are urgently needed. Immunotherapy, particularly the blockade of inhibitory immune checkpoints, is a leading treatment option in cancer and autoimmunity. In this study, we used a murine model of Salmonella Typhimurium infection to investigate whether immune checkpoint blockade could be applied to bacterial infection. We found that the immune checkpoint T-cell immunoglobulin and ITIM domain (TIGIT) was significantly upregulated on lymphocytes during infection, particularly on CD4+ T cells, drastically limiting their proinflammatory function. Blockade of TIGIT in vivo using monoclonal antibodies was able to enhance immunity and improve bacterial clearance. The efficacy of anti-TIGIT was dependent on the capacity of the antibody to bind to Fc (fragment crystallizable) receptors, giving important insights into the mechanism of anti-TIGIT therapy. This research suggests that targeting immune checkpoints, such as TIGIT, has the potential to enhance immune responses toward bacteria and restore antibacterial treatment options in the face of antibiotic resistance. In this experiment, we investigated the effect of TIGIT on CD4+ T cells by performing bulk RNA-sequencing on WT or TIGIT-/- CD4+ T cells in the context of S. Typhimurium infection.

2024-10-31 | GSE234086 | GEO

TIGIT+ iTregs elicited by human regulatory macrophages control T cell immunity

Project description:Human regulatory macrophages (Mreg) have shown early clinical promise as a cell-based, adjunct immunosuppressive therapy in solid organ transplantation. It is hypothesised that recipient CD4+ T cell responses are actively regulated through direct allorecognition of donor-derived Mregs. Here we show that human Mregs convert allogeneic CD4+ T cells to IL-10-producing, TIGIT+ FoxP3+ induced regulatory T cells that non-specifically suppress bystander T cells and inhibit dendritic cell maturation. Differentiation of Mreg-induced Tregs (miTregs) relies on multiple, non-redundant mechanisms that are not exclusive to interaction of Mregs and T cells, including signals mediated by indoleamine 2,3-dioxygenase, TGF-β, retinoic acid, Notch and progestagen-associated endometrial protein. Preoperative administration of donor-derived Mregs to living-donor kidney transplant recipients results in an acute increase in circulating TIGIT+ Tregs. These results suggest a feed-forward mechanism by which Mreg treatment promotes allograft acceptance through rapid induction of direct pathway Tregs.

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TIGIT+ Tregs

2014-12-12 | GSE56299 | GEO

Dual T cell– and B cell–intrinsic deficiency in humans [CD4+ T cell SubSeries]

Project description:Dual T cell– and B cell–intrinsic deficiency in humans [CD4+ T cell SubSeries]

| PRJNA717109 | ENA

Effect of NIK overexpression on Foxp3+CD4+ and Foxp3-CD4+ T cell subsets

Project description:Effect of NIK overexpression on Foxp3+CD4+ and Foxp3-CD4+ T cell subsets

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Metabolomics Analysis of the Effect of GAT-2 Deficiency on Th1 Cells in Mice

Project description:<p>The classic neurotransmitter gamma-aminobutyric acid (GABA) has been shown to shape the activation and function of immune cells. There are four high affinity GABA transporters (GATs, including GAT-1, GAT-2, GAT-3 and GAT-4) responsible for the transmembrane transport of GABA in mice. To explore the effect of GAT-2 on type 1 helper T (Th1) cells, naïve CD4+ T cells were isolated from splenocytes of GAT-2 knockout (KO) and wild-type (WT) mice and cultured for Th1 cell differentiation, and then metabolomics analysis of Th1 cells was performed via gas chromatography coupled to time-of-flight mass spectrometry (GC-TOF-MS) added with multivariate analyses. The study will provide insights into T cell response to GAT-2 deficiency in mice.</p>

2021-10-14 | MTBLS3358 | MetaboLights

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