Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA717109 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14059800_1.fastq.gz	Fastqsanger.gz
	SRR14059800_2.fastq.gz	Fastqsanger.gz
	SRR14059801_1.fastq.gz	Fastqsanger.gz
	SRR14059801_2.fastq.gz	Fastqsanger.gz
	SRR14059802_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 150

Similar Datasets

Dual T cell– and B cell–intrinsic deficiency in humans

Project description:Dual T cell– and B cell–intrinsic deficiency in humans

| PRJNA716960 | ENA

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

Project description:Human RLTPR deficiency is a combined immunodeficiency affecting the CD28-responsive pathway in T cells and the BCR-responsive pathway in B cells. This SubSeries contains high throughput gene expression data from primary CD4+ T cells of patients with RLTPR deficiency and controls.

2022-11-07 | GSE169506 | GEO

Dual T cell– and B cell–intrinsic deficiency in humans

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

2022-11-07 | GSE169508 | GEO

Dual T cell- and B cell-intrinsic deficiency in humans with biallelic RLTPR mutations.

Project description:Combined immunodeficiency (CID) refers to inborn errors of human T cells that also affect B cells because of the T cell deficit or an additional B cell-intrinsic deficit. In this study, we report six patients from three unrelated families with biallelic loss-of-function mutations in RLTPR, the mouse orthologue of which is essential for CD28 signaling. The patients have cutaneous and pulmonary allergy, as well as a variety of bacterial and fungal infectious diseases, including invasive tuberculosis and mucocutaneous candidiasis. Proportions of circulating regulatory T cells and memory CD4+ T cells are reduced. Their CD4+ T cells do not respond to CD28 stimulation. Their CD4+ T cells exhibit a "Th2" cell bias ex vivo and when cultured in vitro, contrasting with the paucity of "Th1," "Th17," and T follicular helper cells. The patients also display few memory B cells and poor antibody responses. This B cell phenotype does not result solely from the T cell deficiency, as the patients' B cells fail to activate NF-?B upon B cell receptor (BCR) stimulation. Human RLTPR deficiency is a CID affecting at least the CD28-responsive pathway in T cells and the BCR-responsive pathway in B cells.

| S-EPMC5068239 | biostudies-literature

IEC intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation

Project description:IEC intrinsic IL-1R signaling holds dual roles in regulating intestinal homeostasis and inflammation

| PRJNA795516 | ENA

Inhibiting tumor cell-intrinsic UBA6 by inosine augments tumor immunogenicity

Project description:Metabolic alteration influences cancer immunity. However, the role and mechanism of metabolic adaption on immune checkpoint blockade (ICB) responses remains ill-defined. Here, metabolomic profiling in mouse tumor models and cancer patients treated with ICB was performed. We found that metabolite inosine was associated with ICB sensitivity in mice and humans, and overcame ICB resistance in several mouse tumor models. Notably, inosine sensitized tumor cells to T cell-mediated cytotoxicity by amplifying tumor-intrinsic immunogenicity. Chemical proteomics further identified that inosine directly bound and inhibited ubiquitin-activating enzyme UBA6. Tumor intrinsic UBA6 loss augmented tumor immunogenicity and substituted the synergistic effect of inosine in combination with ICB. Clinically, tumor UBA6 expression negatively correlated with ICB response in cancer patients. Thus, we reveal an unappreciated function of inosine on tumor-intrinsic immunogenicity and UBA6 as a candidate target for immunotherapy.

2022-08-04 | GSE210225 | GEO

Latent HIV infection disrupts cell-intrinsic innate immunity

Project description:Latent HIV infection disrupts cell-intrinsic innate immunity

| PRJNA729655 | ENA

Cancer-cell intrinsic electrical activity drives small-cell lung cancer progression

Project description:Cancer-cell intrinsic electrical activity drives small-cell lung cancer progression

| PRJNA1126122 | ENA

Dual targeting of polyamine synthesis and uptake in diffuse intrinsic pontine gliomas

Project description:Diffuse intrinsic pontine glioma (DIPG) is an incurable malignant childhood brain tumour, with no active systemic therapies and a 5-year survival of less than 1%. Polyamines are small organic polycations that are essential for DNA replication, translation and cell proliferation. Ornithine decarboxylase 1 (ODC1), the rate limiting enzyme in polyamine synthesis, is irreversibly inhibited by difluoromethylornithine (DFMO). Herein we show that polyamine synthesis is upregulated in DIPG, leading to sensitivity to DFMO. DIPG cells compensate for ODC1 inhibition by upregulation of the polyamine transporter SLC3A2. Treatment with the polyamine transporter inhibitor AMXT 1501 reduced uptake of polyamines in DIPG cells, and co-administration of AMXT 1501 and DFMO led to potent in vitro activity, and significant extension of survival in three aggressive DIPG orthotopic animal models. Collectively, these results demonstrate the potential of dual targeting of polyamine synthesis and uptake as a therapeutic strategy for incurable DIPG.

| EGAS00001004905 | EGA

Dual RNA-seq – Pilot Dual RNA-seq

Project description:Dual RNA-seq – Pilot Dual RNA-seq

| PRJNA280840 | ENA