Pre-GC and GC B cell scRNAseq
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA973113 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24601817.fastq.gz | Fastqsanger.gz | |||
| SRR24601818.fastq.gz | Fastqsanger.gz | |||
| SRR24601819.fastq.gz | Fastqsanger.gz | |||
| SRR24601820.fastq.gz | Fastqsanger.gz | |||
| SRR24601821.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 10 |
Similar Datasets
Project description:Following infection or vaccination, activated B cells at extrafollicular sites or within germinal centers (GCs) undergo vigorous clonal proliferation. Proliferating lymphocytes have been shown to undertake lactate dehydrogenase A (LDHA)-dependent aerobic glycolysis; however, the specific role of this metabolic pathway in a B cell transitioning from a naïve to a highly proliferative, activated state remains poorly defined. Here, we deleted LDHA in a stage- and cell-specific manner. We find that ablation of LDHA in a naïve B cell did not profoundly affect its ability to undergo a T cell-independent extrafollicular B cell response. On the other hand, LDHA-deleted naïve B cells had a severe defect in the capacities to form GCs and mount GC-dependent antibody responses. In addition, loss of LDHA in T cells severely compromised B cell-dependent immune responses. Strikingly, when LDHA was deleted in activated, as opposed to naïve, B cells, there were only minimal effects on the GC reaction and in the generation of high-affinity antibodies. These findings strongly suggest that naïve and activated B cells have distinct metabolic requirements that are further regulated by niche and cellular interactions.
2023-05-21 | GSE232659 | GEO
Project description:GEP on Affymetrix Genechip HTA 2.0 microarrays was performed on ex vivo cell-sorted GC-Tfh and pre-Tfh from TONS and FL
2020-09-16 | GSE157801 | GEO
Project description:We analyzed transcriptome differences of antigen-specific pre-GC B cells. We transferred wildtype (CD4-Cre) or BCL6-insufficient (CD4-CrexBcl6fl/+) OT-II T cells into SAP-deficient mice and immunized these mice with NP-OVA. By day 3 post immunization, we sort-purified NP-binding B cells that were developing into GCs and conducted RNA-seq analyses of their transcriptome. NP+IgDlowB220+ pre-GC B cells from recipients of the same group were pooled to sort-purify 4 200-cell repeats. Using a gene expression signature induced by CD40 signaling in B cells for enrichment analysis, we found such CD40-induced gene set expression was significantly deprived in those NP-binding B cells helped by CD4-Cre´Bcl6fl/+ T cells. These data suggest BCL6 insufficiency in T cells leads to impaired CD40L signaling to B cells.
2021-07-30 | GSE180833 | GEO
Project description:Relative protein quantification of RPL4 and RPL39L in non-ribosome, 40S, 60S and ribosome fractions by PRM;Absolute quantification of RPL39 and RPL39L levels in ribosomes of GC-1 wild type cell, and RPL39L-IRES-eGFP-overexpressed RibosomeCore-/Y GC-1 cells with or without dox-induced expression of RPL39 by PRM. Bovine serum albumin (BSA) as a negative control.
2022-10-19 | PXD037257 | Pride
Project description:LZ and DZ GC B cell throughout lupus
| PRJNA1054613 | ENA
Project description:The study aims to explore gene expression changes associated with commerically available germ cell lines, GC-1 (spg) and GC-2 (spd)ts
2021-06-24 | GSE171224 | GEO
Project description:Revisiting the characteristics of testicular germ cell lines GC-1(spg) and GC-2(spd)ts
| PRJNA718822 | ENA
Project description:Differentiating B cells in germinal centers (GC) require tightly coordinated transcriptional and epigenetic transitions to generate efficient humoral immune responses. The mammalian BAF (Brg1/Brm-associated factor) complexes are major regulators of nucleosomal remodeling, crucial for cellular differentiation and development, and are commonly mutated in several cancers, including GC-derived B cell lymphomas. However, the specific roles of distinct BAF complexes in GC B cell biology and the generation of functional humoral immune responses are not well-understood. Here, we show that the Arid1a-dependent canonical BAF (cBAF) complex is indispensable for generatingon of fully mature GCs and high affinity humoral immune responses. While Arid1a-deficient B cells undergo activation to initiate GC responses, they fail to sustain the GC program, resulting incausing premature GC collapse. Mechanistically, Arid1a-dependent cBAF activity establishes permissive chromatin landscapes at several thousand genomic regions during B cell activation and isare concomitantly required to suppress inflammatory gene programs to maintain transcriptional fidelity in early GC B cells. Interestingly, the inflammatory signatures instigated by Arid1a- deficiency in early GC B cells recruits neutrophils and inflammatory monocytes, and eventually disrupts GC homeostasis. Remarkably, dampening of inflammatory cues with anti-inflammatory glucocorticoid receptor signaling rescues GC B cell differentiation of Arid1a-deficient B cells, thus highlighting a critical role of inflammation in impeding GC responses. In sum, our work identifies essential functions of Arid1a-dependent BAF activity in promoting efficient GC responses. These findings further support recent paradigms uncovering a deterministic role of unrestrained inflammation in obstructing GC responses, common in patients with severe bacterial and viral infections.
2024-02-14 | GSE246912 | GEO
Project description:Differentiating B cells in germinal centers (GC) require tightly coordinated transcriptional and epigenetic transitions to generate efficient humoral immune responses. The mammalian BAF (Brg1/Brm-associated factor) complexes are major regulators of nucleosomal remodeling, crucial for cellular differentiation and development, and are commonly mutated in several cancers, including GC-derived B cell lymphomas. However, the specific roles of distinct BAF complexes in GC B cell biology and the generation of functional humoral immune responses are not well-understood. Here, we show that the Arid1a-dependent canonical BAF (cBAF) complex is indispensable for generatingon of fully mature GCs and high affinity humoral immune responses. While Arid1a-deficient B cells undergo activation to initiate GC responses, they fail to sustain the GC program, resulting incausing premature GC collapse. Mechanistically, Arid1a-dependent cBAF activity establishes permissive chromatin landscapes at several thousand genomic regions during B cell activation and isare concomitantly required to suppress inflammatory gene programs to maintain transcriptional fidelity in early GC B cells. Interestingly, the inflammatory signatures instigated by Arid1a- deficiency in early GC B cells recruits neutrophils and inflammatory monocytes, and eventually disrupts GC homeostasis. Remarkably, dampening of inflammatory cues with anti-inflammatory glucocorticoid receptor signaling rescues GC B cell differentiation of Arid1a-deficient B cells, thus highlighting a critical role of inflammation in impeding GC responses. In sum, our work identifies essential functions of Arid1a-dependent BAF activity in promoting efficient GC responses. These findings further support recent paradigms uncovering a deterministic role of unrestrained inflammation in obstructing GC responses, common in patients with severe bacterial and viral infections.
2024-07-31 | GSE267944 | GEO