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Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria (ATAC-seq)

ABSTRACT: Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria (ATAC-seq)

PROVIDER: PRJNA494312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7948430_1.fastq.gz	Fastqsanger.gz
	SRR7948430_2.fastq.gz	Fastqsanger.gz
	SRR7948431_1.fastq.gz	Fastqsanger.gz
	SRR7948431_2.fastq.gz	Fastqsanger.gz
	SRR7948429_1.fastq.gz	Fastqsanger.gz

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Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria

Project description:Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria

| PRJNA494310 | ENA

Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria (ATAC-seq)

Project description:Despite the key role that antibodies play in protection against malaria, the cellular processes modulating the acquisition of immunity are not fully understood. Using an infection model of severe malaria, we found that GC B cells strongly upregulate the transcription factor T-bet in response to infection. Expression of T-bet in B cells was required for IgG2c switching but reduced the magnitude of GC B cell responses. RNA-sequencing and flow cytometry analysis revealed that T-bet supports a transcriptional program resulting in a substantial enrichment of the GC dark zone (DZ), thereby significantly influencing DZ/light zone (LZ) polarization. Mice deficient in T-bet in their B cells displayed significantly reduced affinity mutation frequencies in their IghV genes and lower antibody avidity than controls, indicating that T-bet modulates affinity maturation. These results demonstrate that T-bet promotes appropriate GC dynamics, thereby leading to the differentiation of B cells with increased affinity for antigen.

2019-11-11 | GSE120727 | GEO

Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria (RNA-seq)

2019-11-11 | GSE120728 | GEO

Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria (RNA-seq)

Project description:Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria (RNA-seq)

| PRJNA494311 | ENA

Gene expression profiling in RagC Q119L germinal centre B cells

Project description:Gene expression by RNAseq in murine RagC Q119L/+ and RagC +/+ germinal centre B cells

2021-07-13 | GSE174003 | GEO

Transcription factor T-bet in B cells controls germinal centre polarization and antibody affinity maturation in response to malaria

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

2019-11-11 | GSE120729 | GEO

Dynamic mitochondrial transcription and translation in B cells control germinal centre entry and lymphomagenesis

Project description:Study of the effects of Tfam deletion on germinal centre B cells

2022-07-19 | GSE208021 | GEO

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

2007-09-05 | GSE8906 | GEO

Role of affinity in plasma cell development in the germinal center light zone

Project description:Protective immune responses to many pathogens depend on the development of high affinity antibody-producing plasma cells in germinal centers. Transgenic models suggest that there is a stringent affinity-based barrier to plasma cell development. Whether a similar high affinity barrier regulates plasma cell development under physiologic circumstances, and the nature of the plasma cell fate decision has not been defined precisely. Here we use a fate mapping approach to examine the relationship between germinal center (GC) B cells selected to undergo additional rounds of affinity maturation, germinal center pre-plasma cells and plasma cells. The data show that initial plasma cell selection overlaps with germinal center B cell selection, but that the plasma cell compartment accumulates a less diverse and higher affinity collection of antibodies over time. Thus, whereas the GC continues to diversify over time, affinity-based pre-plasma cell selection sieves the germinal center to enable accumulation of a more restricted group of high affinity antibody secreting plasma cells.

2023-11-02 | GSE246382 | GEO

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.

2021-09-22 | GSE145413 | GEO

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