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Isotype switching in human memory B cells sets intrinsic antigen-affinity thresholds that dictate antigen-driven fates

ABSTRACT: Isotype switching in human memory B cells sets intrinsic antigen-affinity thresholds that dictate antigen-driven fates

PROVIDER: PRJNA890611 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21905007_1.fastq.gz	Fastqsanger.gz
	SRR21905007_2.fastq.gz	Fastqsanger.gz
	SRR21905008_1.fastq.gz	Fastqsanger.gz
	SRR21905008_2.fastq.gz	Fastqsanger.gz
	SRR21905009_1.fastq.gz	Fastqsanger.gz

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Isotype switching in human memory B cells sets intrinsic antigen-affinity thresholds that dictate antigen-driven fates

Project description:Memory B cells (MBCs) play a critical role in protection against homologous and variant pathogen challenge by either differentiating to plasma cells (PCs) or to germinal center (GCs) B cells. The human MBC compartment contains both switched IgG+ and unswitched IgM+ MBCs and at present the contribution of these MBC subpopulations to protection is incompletely understood. We discovered that intrinsic antigen-affinity thresholds for activation were at least 100-fold higher for IgG+ as compared to IgM+ MBCs and that IgG+ MBCs when challenged responded only to high affinity antigens and differentiated almost exclusively towards PC fates. In contrast, IgM+ MBCs were eliminated by apoptosis by high affinity antigens and responded to low affinity antigens by differentiating towards GC B cell fates. Thus, IgG+ and IgM+ MBCs may play distinct yet complementary roles in response to pathogen challenge to ensure the immediate production of high affinity antibodies to homologous and closely related challenges and the generation of variant-specific MBCs through GC reactions.

2023-10-25 | GSE215788 | GEO

Isotype-specific plasma cells express divergent transcriptional programs

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Small protein modules dictate prophage fates during polylysogeny.

Project description:Most bacteria in the biosphere are predicted to be polylysogens harbouring multiple prophages1-5. In studied systems, prophage induction from lysogeny to lysis is near-universally driven by DNA-damaging agents6. Thus, how co-residing prophages compete for cell resources if they respond to an identical trigger is unknown. Here we discover regulatory modules that control prophage induction independently of the DNA-damage cue. The modules bear little resemblance at the sequence level but share a regulatory logic by having a transcription factor that activates the expression of a neighbouring gene that encodes a small protein. The small protein inactivates the master repressor of lysis, which leads to induction. Polylysogens that harbour two prophages exposed to DNA damage release mixed populations of phages. Single-cell analyses reveal that this blend is a consequence of discrete subsets of cells producing one, the other or both phages. By contrast, induction through the DNA-damage-independent module results in cells producing only the phage sensitive to that specific cue. Thus, in the polylysogens tested, the stimulus used to induce lysis determines phage productivity. Considering the lack of potent DNA-damaging agents in natural habitats, additional phage-encoded sensory pathways to lysis likely have fundamental roles in phage-host biology and inter-prophage competition.

| S-EPMC10432266 | biostudies-literature

CpG islands and GC content dictate nucleosome depletion in a transcription independent manner at mammalian promoters

Project description:This SuperSeries is composed of the following subset Series: GSE38560: CpG islands and GC content dictate nucleosome depletion in a transcription independent manner at mammalian promoters (RNA-seq) GSE38561: CpG islands and GC content dictate nucleosome depletion in a transcription independent manner at mammalian promoters (ChIP-seq) GSE38562: CpG islands and GC content dictate nucleosome depletion in a transcription independent manner at mammalian promoters (genomic SEQ) GSE38563: CpG islands and GC content dictate nucleosome depletion in a transcription independent manner at mammalian promoters (MNase-seq) GSE38564: CpG islands and GC content dictate nucleosome depletion in a transcription independent manner at mammalian promoters (5) Refer to individual Series

2012-06-11 | E-GEOD-38577 | biostudies-arrayexpress

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IgH Isotype-Specific B Cell Receptor Dosage Regulates B Cell Fate

Project description:We use polyclonal Ighγ1/γ1 and Ighε/ε mice (which initially produce only IgG1 or IgE from their respective native genomic configurations) to examine the role of IgH isotype on BCR function. We use microarray expression analysis to compare the internal state of the three IgH isotype specific B-cells. Microarray was used to compare the expression level of various genes in splenic follicular B-cells of Ighε/ε, Ighγ1/γ1 and Ighwt mice. Each mouse strain also had a naturally pre-assembled Ig light chain (VJk5).

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Human B cell isotype switching origins of IgE

Project description:Human B cell isotype switching origins of IgE

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Isotype-specific plasma cells express divergent transcriptional programs

Project description:Isotype-specific plasma cells express divergent transcriptional programs

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Isotype-based plasma cell subsets display differential niches requirements in the bone marrow

Project description:Bone marrow long-lived plasma cells are essential for long-term protection against infection and their persistence within this organ relies on interactions with Cxcl12-expressing stromal cells that are still not clearly identified. Here, using single cell RNAseq and in silico transinteractome analyses we identified LepR+ mesenchymal cells as the stromal cell subset most likely to interact with plasma cells within the bone marrow. Moreover, we demonstrated that depending on the isotype they express, plasma cells may use different set of integrins and adhesion molecules to interact with these stromal cells. Altogether, our results constitute an unprecedented characterization of plasma cell subset stromal niches and open new avenues for the specific targeting of bone marrow plasma cells based on their isotype.

2023-06-30 | GSE228543 | GEO

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