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Single-cell genomics predict germinal centre-associated etiology of autoimmune risk loci

ABSTRACT: Single-cell genomics predict germinal centre-associated etiology of autoimmune risk loci

PROVIDER: PRJNA698360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR13592261.fastq.gz	Fastqsanger.gz
	SRR13592262.fastq.gz	Fastqsanger.gz
	SRR13592263.fastq.gz	Fastqsanger.gz
	SRR13592264.fastq.gz	Fastqsanger.gz

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Single-cell genomics predict germinal centre-associated etiology of autoimmune risk loci

Project description:The germinal centre (GC) response is critical for both effective adaptive immune responses and establishing peripheral tolerance by limiting auto-reactive B cells. To understand the gene regulatory principles underlying B cell maturation and the GC response we generated a single-cell transcriptomic and epigenomic atlas of the human tonsil, a widely studied, representative lymphoid tissue. We identify diverse immune cell subsets to help us map dynamic transcription factor activity during B cell activation, GC formation and plasma cell differentiation. We subsequently leverage cell type-specific transcriptomic and epigenomic maps to interpret the regulatory potential of fine-mapped autoimmune genetic variants. This reveals that many autoimmune disease-associated variants exhibit the greatest regulatory potential in GC-associated immune cell populations, providing a valuable cell-type resolved resource to understanding cellular and genetic causes underpinning autoimmune disease.

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Gene expression profiling in RagC Q119L germinal centre B cells

Project description:Gene expression profiling in RagC Q119L germinal centre B cells

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Effect of B cell-intrinsic deletion of MLL1 on gene expression of germinal centre B cells during day 13 Trichuris muris infection

Project description:We measured the gene expression differences in germinal centre B cells from day 13 Trichuris muris-infected mice in which MLL1 is conditionally deleted in mature B cells

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Comparative gene expression profiles of T-dependent and T-independent germinal centre B cells in mice

Project description:Selection of B cells subjected to hypermutation in germinal centres (GC) during T-dependent (TD) antibody responses yields memory cells and long-lived plasma cells that produce high affinity antibodies biased to foreign antigens rather than self-antigens. GC also form in T-independent (TI) responses to polysaccharide antigens but failed selection results in GC involution and memory cells are not generated. To date there are no markers that allow phenotypic distinction of T-dependent and T-independent germinal centre B cells. We have now compared the global gene expression of GC B cells purified from mice immunized with either TD or TI antigens and identified eighty genes that are differentially expressed in TD GC. Keywords: T-dependent and T-independent germinal center B cells

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Transcriptomic analysis of in vitro induced germinal centre-like B cells and plasmablast differentiation

Project description:To elucidate molecular mechanisms that regulate the terminal differentiation of B cells into plasmablasts, we analysed how the B cell transcriptome changes during an in vitro culture system that mimics the germinal centre response (known as iGB culture). By culturing B cells on feeder cells expressing CD40L and B-cell activating factor BAFF in the presence of interleukin 4 and interleukin 21, this system allows class switch recombination to IgG1-producing cells and formation of CD138+ TACI+ B220low CD19int/low plasmablasts.

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Integrated single-cell transcriptomics and epigenomics reveals strong germinal center-associated etiology of autoimmune risk loci.

Project description:The germinal center (GC) response is critical for both effective adaptive immunity and establishing peripheral tolerance by limiting autoreactive B cells. Dysfunction in these processes can lead to defective immune responses to infection or contribute to autoimmune disease. To understand the gene regulatory principles underlying the GC response, we generated a single-cell transcriptomic and epigenomic atlas of the human tonsil, a widely studied and representative lymphoid tissue. We characterize diverse immune cell subsets and build a trajectory of dynamic gene expression and transcription factor activity during B cell activation, GC formation, and plasma cell differentiation. We subsequently leverage cell type–specific transcriptomic and epigenomic maps to interpret potential regulatory impact of genetic variants implicated in autoimmunity, revealing that many exhibit their greatest regulatory potential in GC-associated cellular populations. These included gene loci linked with known roles in GC biology (IL21, IL21R, IL4R, and BCL6) and transcription factors regulating B cell differentiation (POU2AF1 and HHEX). Together, these analyses provide a powerful new cell type–resolved resource for the interpretation of cellular and genetic causes underpinning autoimmune disease.

| S-EPMC8859880 | biostudies-literature

The RNA binding proteins TIA1 and TIAL1 protect germinal centre responses from apoptosis

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The RNA-binding protein HuR is required for antigen-specific germinal centre B cell selection.

Project description:The germinal centre (GC) is a hallmark of adaptive immunity. Gene expression in GCs is tightly regulated but the impact of post-transcriptional mechanisms are largely unknown. Here we show that expression of the RNA binding protein HuR is essential in GCs. In its absence, GC B cells are at a competitive disadvantage and high-affinity antibody production is severely impaired. Mechanistically, HuR affects the transcriptome qualitatively and quantitatively to enable the expression of a Myc- dependent transcriptional program essential for light zone B cells to re-enter into the dark zone for further proliferation and Ig somatic hypermutation. HuR controls the splicing and abundance of mRNAs required for entry into and transition through the S phase of the cell cycle. HuR modulates a gene signature associated with DNA deamination preserving GC B cells from extensive DNA damage and cell death.

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