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Analysis of transcriptomes of germinal center (GC) B cells derived from miR-155-sufficient and -deficient mice at the single-cell level [scRNA-seq]

ABSTRACT: To investigate the impact caused by miR-155 ablation, GC B cells were sorted by flow cytometry and used to analyze transcriptomic profiles.

ORGANISM(S): Mus musculus

PROVIDER: GSE230528 | GEO | 2024/10/29

REPOSITORIES: GEO

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Analysis of transcriptomes of germinal center (GC) B cells derived from miR-155-sufficient and -deficient mice

Project description:To investigate the impact caused by miR-155 ablation, positively selected light zone (LZ) GC B cells were sorted by flow cytometry and used to analyse transcriptomic profiles.

2024-11-01 | GSE231649 | GEO

Analysis of transcriptomes of germinal center (GC) B cells derived from miR-155-sufficient and -deficient mice

Project description:Analysis of transcriptomes of germinal center (GC) B cells derived from miR-155-sufficient and -deficient mice

| PRJNA967244 | ENA

Analysis of transcriptomes of germinal center (GC) B cells derived from miR-155-sufficient and -deficient mice at the single-cell level [scRNA-seq]

Project description:Analysis of transcriptomes of germinal center (GC) B cells derived from miR-155-sufficient and -deficient mice at the single-cell level [scRNA-seq]

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Genome-wide profiling of Kdm2a binding and H3K36me2 of hypoxia-cultured B cells derived from miR-155-sufficient and -deficient mice [ChIP-seq]

Project description:To investigate the impact caused by miR-155 ablation, B cells from miR-155-sufficient and -deficient mice were cultured in hypoxic conditions and analyzed for profiling the binding of a miR-155 target, Kdm2a, to genomic loci and the distribution pattern of H3K36me2, which Kdm2a demethylates.

2024-10-30 | GSE230527 | GEO

Transcriptional profiling of murine germinal center (GC) B cells from GC-specific conditional Crebbp and Ep300 knock-out mice

Project description:Inactivating mutations of the CREBBP acetyltransferase and, at lower frequencies, its paralogue EP300 are among the most common genetic alterations in diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL), the two most frequent B cell malignancies. Here we uncover unexpected distinct functions for CREBBP and EP300 in the germinal center (GC), i.e. the target structure for most human B cell lymphomas. We show that these proteins modulate non-overlapping transcriptional programs that are preferentially enriched in biological functions associated with the separate anatomic compartments of the GC. Consistently, deletion of CREBBP or EP300 have opposing effects on GC formation in vivo. Nonetheless, these proteins partially compensate for each other to maintain a minimal threshold of acetyltransferase activity and guarantee homeostatic control of the GC, which is completely abrogated by their combined loss. This synthetic lethal interaction is retained in DLBCL cells, identifying an Achille’s heel in CREBBP-mutant lymphomas that could be pharmacologically targeted by using a novel, selective small molecule inhibitor of the CREBBP/EP300 bromodomain. These data shed light on the unique roles of CREBBP and EP300 in the physiology and pathology of GC B cells, and provide a proof-of-principle for the development and testing of EP300 inhibition as a therapeutic strategy in these diseases.

2021-06-01 | GSE124192 | GEO

Transcriptional Changes in Germinal Center (GC) B cells from LSD1 conditional knockout mice

Project description:Using RNA-seq we identified the gene expression changes in GC B cells from LSD1 wild-type or LSD1-deficient mice immunized with T cell dependent antigens (Sheep Red Blood cells)

2018-12-10 | GSE106417 | GEO

Germinal Center T follicular helper (GC-Tfh) cell impairment in chronic HIV infection involves c-Maf signaling [microarray]

Project description:We have recently demonstrated that the function of T follicular helper (Tfh) cells obtained from lymph nodes (LN) of HIV-infected individuals is impaired. We found that these cells were unable to provide proper help to germinal center (GC)-B cells, as observed by altered and inefficient anti-HIV antibody response and premature death of memory B cells. The underlying molecular mechanisms of this dysfunction remain poorly defined. Herein, we have used a unique transcriptional approach to identify these molecular defects. We consequently determined the transcriptional profiles of LN GC-Tfh cells following their interactions with LN GC-B cells from HIV-infected and HIV-uninfected individuals, rather than analyzing resting ex-vivo GC-Tfh cells. We observed that proliferating HIV-infected GC-Tfh cells were transcriptionally different than those from HIV-uninfected individuals, displaying a significant downregulation of immune- and GC-Tfh-associated pathways and genes compared to cells from uninfected individuals. Our results strongly demonstrated that MAF (coding for the transcription factor c-Maf) and its upstream signaling pathway mediators (IL6R and STAT3) were significantly downregulated in HIV-infected subjects, which could contribute to the impaired GC-Tfh and GC-B cell functions reported during infection. We further showed that c-Maf function was associated with the adenosine pathway and that the signaling upstream c-Maf could be partially restored by adenosine deaminase -1 (ADA-1) supplementation. Overall, we identified a novel mechanism that contributes to GC-Tfh impairment during HIV infection. Understanding how GC-Tfh function is altered in HIV is crucial and could provide critical information about the mechanisms leading to the development and maintenance of effective anti-HIV antibodies.

2021-07-19 | GSE175728 | GEO

Germinal Center T follicular helper (GC-Tfh) cell impairment in chronic HIV infection involves c-Maf signaling [RNA-seq]

2021-07-19 | GSE173500 | GEO

MEF2B LC-MS in normal and malignant germinal center B cells.

Project description:The MEF2B transcription factor is frequently mutated in germinal center (GC)-derived B-cell lymphomas. Its N-terminal mutations drive lymphomagenesis by escaping interaction with transcriptional repressors, while the function of C-terminal mutations remains to be elucidated. Here, we show that MEF2B C-tail is physiologically phosphorylated at specific residues and phosphorylation at S324 is impaired by lymphoma-associated mutations. Lack of phosphorylation at S324 enhances the interaction of MEF2B with the SWI/SNF chromatin remodeling complex, leading to higher transcriptional activity. In addition, these mutants show an increased protein stability due to impaired interaction with the CUL3/KLHL12 ubiquitin complex. Mice expressing a phosphorylation-deficient lymphoma-associated MEF2B mutant display GC enlargement and develop GC-derived lymphomas, when crossed with Bcl2 transgenic mice. These results unveil converging mechanisms of action for a diverse spectrum of MEF2B mutations, all leading to its dysregulation and GC B-cell lymphomagenesis. These assorted mechanisms provide additional opportunities for the development of targeted therapeutic approaches.

2024-08-26 | PXD043998 | Pride

SENP1 Regulates Germinal Center B Cell Responses through PAX5-deSUMOylation mediated AID expression

Project description:Humoral immunity depends on germinal center reaction where B cells are tightly controlled for class switch recombination (CSR) and somatic hypermutation, and finally generated into plasma and memory B cells. However, how protein SUMOylation control the key events of GC B cells remains to be understood. Here, we show that SUMO-specific protease 1 (SENP1) is upregulated in GC B cells. Selective ablation of Senp1 within GC B cells led to defective dark zone versus light zone GC B organization, impaired IgG1-switched GC B cells, and compromised antibody response. In addition, the formation of antigen-specific plasma and memory B cells were also diminished when SENP1 was deleted in GC B cells. Mechanistically, SENP1 was indispensable for expression of activation-induced cytidine deaminase (AID). SENP1-mediated Paired box protein 5 deSUMOylation suppressed the transcription to AID, which might be responsible for defective CSR in vivo. Our study not only established the importance of protein SUMOylation for the maintenance of GC B cell function but also clarified a novel mechanism to the modulation of AID expression.

2024-06-12 | GSE227067 | GEO

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