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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE205101 | GEO | 2022/07/05

REPOSITORIES: GEO

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

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 | GSE173644 | GEO

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

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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

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

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

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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]

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Project description:Time-restricted feeding (TRF) has recently gained interest as a potential anti-ageing treatment for organisms from Drosophila to humans1-5. TRF restricts food intake to specific hours of the day. Because TRF controls the timing of feeding, rather than nutrient or caloric content, TRF has been hypothesized to depend on circadian-regulated functions; the underlying molecular mechanisms of its effects remain unclear. Here, to exploit the genetic tools and well-characterized ageing markers of Drosophila, we developed an intermittent TRF (iTRF) dietary regimen that robustly extended fly lifespan and delayed the onset of ageing markers in the muscles and gut. We found that iTRF enhanced circadian-regulated transcription and that iTRF-mediated lifespan extension required both circadian regulation and autophagy, a conserved longevity pathway. Night-specific induction of autophagy was both necessary and sufficient to extend lifespan on an ad libitum diet and also prevented further iTRF-mediated lifespan extension. By contrast, day-specific induction of autophagy did not extend lifespan. Thus, these results identify circadian-regulated autophagy as a critical contributor to iTRF-mediated health benefits in Drosophila. Because both circadian regulation and autophagy are highly conserved processes in human ageing, this work highlights the possibility that behavioural or pharmaceutical interventions that stimulate circadian-regulated autophagy might provide people with similar health benefits, such as delayed ageing and lifespan extension.

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

2017-02-10 | GSE69015 | GEO