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APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity [I]

ABSTRACT: APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity [I]

PROVIDER: PRJNA726526 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14369900.fastq.gz	Fastqsanger.gz
	SRR14369901.fastq.gz	Fastqsanger.gz
	SRR14369902.fastq.gz	Fastqsanger.gz
	SRR14369903.fastq.gz	Fastqsanger.gz
	SRR14369904.fastq.gz	Fastqsanger.gz

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Similar Datasets

APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity [II]

Project description:Antibody secreting cells (ASCs) survive in niche microenvironments, but cellular responses driven by particular niche signals are incompletely defined. The TNF superfamily (TNFSF) member A proliferation-inducing ligand (APRIL) can support the maturation of transitory plasmablasts into long-lived plasma cells. Here we explore the biological programs established by APRIL in human plasmablast. Under conditions allowing the maturation of ex vivo or in vitro generated plasmablasts, we find that APRIL drives activation of ERK, p38 and JNK, accompanied by a classical NFκB response and activation of the AKT/FOXO1 pathway. Time course gene expression data resolve co-ordinated transcriptional responses propagated via immediate early genes and NFκB targets and converging onto modules of genes enriched for MYC-targets and metabolism and cell growth related pathways. This response is shared between APRIL and an alternate TNFSF member CD40L but is not a feature of alternative niche signals delivered by IFNα or SDF1. However, APRIL and CD40L responses also diverge. CD40L drives expression of genes related to the activated B-cell state while APRIL does not. Thus, APRIL establishes a broad foundation for plasma cell longevity with features of cellular refuelling, while being uncoupled from support of the B-cell state.

2022-07-05 | GSE205100 | GEO

APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity [I]

2022-07-05 | GSE173644 | GEO

APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity

Project description:APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity

| PRJNA843729 | ENA

APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity [II]

Project description:APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity [II]

| PRJNA843731 | ENA

APRIL drives a co-ordinated but diverse response as a foundation for plasma cell longevity

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

2022-07-05 | GSE205101 | GEO

APRIL Drives a Coordinated but Diverse Response as a Foundation for Plasma Cell Longevity.

Project description:Ab-secreting cells survive in niche microenvironments, but cellular responses driven by particular niche signals are incompletely defined. The TNF superfamily member a proliferation-inducing ligand (APRIL) can support the maturation of transitory plasmablasts into long-lived plasma cells. In this study, we explore the biological programs established by APRIL in human plasmablasts. Under conditions allowing the maturation of ex vivo- or in vitro-generated plasmablasts, we find that APRIL drives activation of ERK, p38, and JNK, accompanied by a classical NF-κB response and activation of the AKT/FOXO1 pathway. Time-course gene expression data resolve coordinated transcriptional responses propagated via immediate early genes and NF-κB targets and converging onto modules of genes enriched for MYC targets and metabolism/cell growth-related pathways. This response is shared between APRIL and an alternate TNF superfamily member CD40L but is not a feature of alternative niche signals delivered by IFN-α or SDF1. However, APRIL and CD40L responses also diverge. CD40L drives expression of genes related to the activated B cell state whereas APRIL does not. Thus, APRIL establishes a broad foundation for plasma cell longevity with features of cellular refueling while being uncoupled from support of the B cell state.

| S-EPMC7613700 | biostudies-literature

Endogenous B cell TACI-Short-APRIL signaling

Project description:Here we show that TACI-S increases its expression with maturation and colocalizes in the intracellular compartment with the ligand APRIL. APRIL downregulation in human B cells, eliminated class switch. These studies suggest the importance of intracellular APRIL together with TACI-S in maintaining humoral immunity.

2023-09-22 | GSE213981 | GEO

Coreceptor delivery of paracrine APRIL to Golgic BCMA lowers immunogenicity of B-cell lymphoma

Project description:APRIL is involved in the development of B-cell lymphomas. However, in tumors the source of APRIL is paracrine while one signaling receptor, BCMA, is intracellular, raising the question on how APRIL may signal. In fact, tumor cells internalized APRIL via their surface HSPG. Then, APRIL trafficked into endosomes to finally interact with Golgic BCMA, whose sequence harbors strong identities with sorting nexins. Intracellular APRIL/BCMA interactions activated the canonical NF-kB pathway, and mediated from tumor cells an immunosuppressive response including IL-10 upregulation. Absence of APRIL/BCMA interactions impaired tumor growth in mice, and APRIL internalization by tumor cells correlated with a reduced survival for patients. Taken together, the present study elucidates a fully intracellular signaling pathway, key to B-cell lymphoma development.

2018-04-26 | GSE113643 | GEO

BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

Project description:Emerging clinical evidence points to a function for B cell activating factor (BAFF) in pregnancy. However, a direct role for BAFF-axis members including BAFF, the closely related a proliferation-inducing ligand (APRIL), and their respective receptors in pregnancy has not been examined. This study demonstrates that loss of BAFF results in decreased inflammatory responsiveness and decreased susceptibility to inflammation-induced preterm birth (PTB). In contrast, loss of APRIL increases inflammatory responsiveness and susceptibility to PTB. Consistent with overlapping receptor utilization by BAFF and APRIL, deletion of BAFF-axis receptors is not sufficient to modify susceptibility to PTB. Critically, therapeutic administration of BAFF/APRIL monoclonal antibodies or recombinant proteins is sufficient to manipulate susceptibility to inflammation-induced PTB. Further, macrophages are identified as the principle BAFF producing immune cells at the maternal-fetal interface and BAFF and APRIL divergently manipulate macrophage gene expression and inflammatory function. Genes linked to labor initiation are upregulated in WT and APRIL deficient macrophages while downregulated in BAFF deficient macrophages and correlate with myeloid gene expression in human placental samples during labor. Thus, BAFF and APRIL play important, but divergent, counterregulatory inflammatory roles in pregnancy and provide new therapeutic targets for mitigating the risk of PTB.

2023-08-03 | GSE202811 | GEO

Time-course effect of APRIL on gene expression in HepG2 cells

Project description:APRIL (TNFSF13) is a ligand of the TNF superfamily which binds to two receptors, BCMA and TACI. We have found that APRIL and its receptor BCMA are specifically enhanced in hepatocellular carcinoma, as compared to non-cancerous liver tissue. We further identified that HepG2 cells present the same ligand/receptor pattern as human hepatocellular carcinomas. We investigated the role of APRIL in HepG2 gene expression in a time course study.

2011-05-20 | GSE29375 | GEO

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