Whole Transcriptome RNASeq Data for Cell-Sorted Antibody Secreting Cells (ASC)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA480714 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7512010.fastq.gz | Fastqsanger.gz | |||
| SRR7512020.fastq.gz | Fastqsanger.gz | |||
| SRR7512011.fastq.gz | Fastqsanger.gz | |||
| SRR7512021.fastq.gz | Fastqsanger.gz | |||
| SRR7512012.fastq.gz | Fastqsanger.gz |
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Project description:Here we describe the dynamics underlying the generation of IgE-antibody secreting cells (ASC) in human nasal polyps (NP), mucosal tissues rich in ASC without germinal centers (GC). Using VH next generation sequencing, we identified an extrafollicular (EF) mucosal IgD+ naïve-like intermediate B cell population with high connectivity to the mucosal IgE ASC. Mucosal IgD+ B cells, express germline epsilon transcripts and predominantly co-express IgM. However, a small but significant fraction co-express IgG or IgA instead which also show connectivity to ASC IgE. Phenotypically, NP IgD+ B cells display an activated profile and molecular evidence of BCR engagement. Transcriptionally, mucosal IgD+ B cells reveal an intermediate profile between naïve B cells and ASC. Single cell IgE ASC analysis demonstrates lower mutational frequencies relative to IgG, IgA, and IgD ASC consistent with IgE ASC derivation from mucosal IgD+ B cell with low mutational load. In conclusion, we describe a novel mechanism of GC-independent, extrafollicular IgE ASC formation at the nasal mucosa whereby activated IgD+ naïve B cells locally undergo direct and indirect (through IgG and IgA), IgE class-switch.
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Project description:Antibody secreting cells (ASC) circulate after vaccination and infection and migrate to the bone marrow (BM) where a subset known as long-lived plasma cells (LLPC) persist and secrete antibodies for a lifetime. The mechanisms of how circulating ASC become LLPC is not well elucidated. Here, we show that human early-minted blood ASCs have distinct morphology, transcriptomes, and epigenetics compared to human BM LLPC. Compared to blood ASC, BM LLPC have decreased nucleus/cytoplasm ratio but increased endoplasmic reticulum and numbers of mitochondria. Additionally, LLPC acquire transcriptional and epigenetic differences in multiple cellular pathways that include apoptosis. Upregulation of the anti-apoptotic genes MCL1, BCL2, BCL-XL while simultaneously downregulation of pro-apoptotic genes HRK1, CASP3, and CASP8 occurs in LLPC. Consistent with the decrease in gene expression, pro-apoptotic gene loci are less accessible in LLPC. In contrast, anti-apoptotic gene expression is increased but is not always accompanied by changes in accessibility. Importantly, we show that early-minted blood ASCs undergo morphological and transcriptional changes that make these cells resemble ex vivo BM ASCs, suggesting that the BM microniche at least in part promotes LLPC maturation. Overall, our study demonstrates that early-minted blood ASC in the BM microniche must undergo morphological, transcriptional, and epigenetic changes to mature into apoptotic-resistant LLPC.
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