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Transcriptional analysis of BCR-triggered immature and mature mouse B cells

ABSTRACT: The B cell antigen receptor (BCR) is a signaling complex that mediates differentiation stage-specific cell fate decisions in B lymphocytes. While several studies have evidenced differences in signal transduction components as being key to contrasting phenotypic outcomes, little is known about the differential BCR-triggered gene transcription. Here we defined transcriptional changes underlying BCR-induced apoptosis and proliferation of immature and mature B cells, respectively. These findings provide the first insights into the early transcriptional events leading to deletion or clonal expansion of B cells upon antigen recognition. Keywords: cell type comparison, development or differentiation design, time course, compound treatment design, microarray experiment record

ORGANISM(S): Mus musculus

PROVIDER: GSE9215 | GEO | 2008/12/15

SECONDARY ACCESSION(S): PRJNA102805

REPOSITORIES: GEO

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Transcriptional analysis of BCR-triggered immature and mature mouse B cells

Project description:The B cell antigen receptor (BCR) is a signaling complex that mediates differentiation stage-specific cell fate decisions in B lymphocytes. While several studies have evidenced differences in signal transduction components as being key to contrasting phenotypic outcomes, little is known about the differential BCR-triggered gene transcription. Here we defined transcriptional changes underlying BCR-induced apoptosis and proliferation of immature and mature B cells, respectively. These findings provide the first insights into the early transcriptional events leading to deletion or clonal expansion of B cells upon antigen recognition. Keywords: cell type comparison, development or differentiation design, time course, compound treatment design, microarray experiment record Total RNA was extracted from immature (IM) and mature (M) B cells both freshly isolated (0h) and stimulated with (BCR) or without (ctrl) anti-μ F(ab’)2 for 2, 8 or 24h. Following RNA extraction, one round of mRNA amplification was applied using the MessageAmpTM Kit (Ambion). All samples, including the amplified Universal Mouse Reference RNA (Stratagene) which served as a reference at each hybridization, were reverse-transcribed and indirectly labeled with Cy3 and Cy5 (Amersham). Quality was controlled by performing 6 or 8 hybridizations of each sample to the cDNA arrays using a dye-swap strategy. 94 arrays were used for hybridization in total.

2008-12-14 | E-GEOD-9215 | biostudies-arrayexpress

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Full-length single-cell BCR sequencing paired with RNA sequencing reveals convergent responses to vaccination

Project description:Single-cell RNA sequencing can to resolve transcriptional features from large numbers of individual immune cells, but techniques capable of resolving the variable regions of B cell receptors (BCR) – defining features that confer antigen specificity to B cells – remain limited, especially from widely-used 3`-barcoded libraries. Here, we report a method that for recovering paired, full-length variable region sequences of the BCRs from 3`-barcoded single-cell whole transcriptome libraries. We first verified this method could produce accurate, full-length BCR sequences. We then applied this method to profile antigen-specific B cell responses elicited against the capsular polysaccharide of Streptococcus pneumoniae serotype 3 (ST3) by glycoconjugate vaccines in infant rhesus macaques. Using our method, we defined features of the BCR associated with specificity for the ST3 antigen and showed that these sequence characteristics are present in multiple vaccinated monkeys, indicating a convergent response to vaccination. These results demonstrate the utility of our method to resolve key features of the B cell repertoire and for profiling antigen-specific responses elicited by vaccination.

2023-05-19 | GSE232873 | GEO

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Project description:BCR ligand-engaged B cells upregulate Nod1 during development. Most mature B cells have up-regulated Nod1 and are sensitive to Nod1 signaling, which increases survival upon exposure to microbial products, as a positive outcome of BCR-engaged mature B cells.

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CEA_SGF:E00010#bcr-abl

Project description:Chronic myelogenous leukemia (CML) is a malignant disease of the hematopoietic stem cell, characterized by the expression of the Bcr-Abl oncogene by leukemic cells. In order to analyze the molecular pathways modulated by Bcr-Abl, we have previously generated an inducible model of Bcr-Abl expression in the murine Ba/F3 cell line based on the Tet-OFF system. In the present study, through a microarray approach applied to cells grown with (Bcr-Abl-expression OFF) or without (Bcr-Abl-expression ON) doxycycline, a tetracycline analogue, we analyzed the gene expression variations upon Bcr-Abl expression. Keywords: repeat sample

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Zfx controls BCR-induced proliferation and survival of B lymphocytes

Project description:The development, homeostasis and function of B lymphocytes involve multiple rounds of B cell receptor (BCR)-controlled proliferation and prolonged maintenance. We analyzed the role of transcription factor Zfx, a recently identified regulator of stem cell maintenance, in B cell development and homeostasis. Conditional Zfx deletion in the bone marrow blocked B cell development at the pre-BCR selection checkpoint. Zfx deficiency in peripheral B cells caused impaired generation of the B-1 cell lineage, accelerated B cell turnover, depletion of mature recirculating cells, and delayed T-dependent antibody responses. Zfx-deficient B cells showed normal proximal BCR signaling, but impaired BCR-induced proliferation and survival. This was accompanied by aberrantly enhanced and prolonged integrated stress response, and delayed induction of Cyclin D2 and Bcl-xL proteins. Thus, Zfx restrains the stress response and couples antigen receptor signaling to B cell expansion and maintenance during development and peripheral homeostasis. Keywords: Expression profiling by array

2009-04-17 | GSE13547 | GEO

Retroviral transduction of CD34+ cells with P190 and P210 BCR/ABL1 fusion genes

Project description:Expression of P190 and P210 BCR/ABL1 in normal human CD34(+) cells induces similar gene expression profiles and results in a STAT5-dependent expansion of the erythroid lineage The P190 and P210 BCR/ABL1 fusion genes are mainly associated with different types of hematologic malignancies, but it is presently unclear whether they are functionally different following expression in primitive human hematopoietic cells. We investigated and systematically compared the effects of retroviral P190 BCR/ABL1 and P210 BCR/ABL1 expression on cell proliferation, differentiation, and global gene expression in human CD34(+) cells from cord blood. Expression of either P190 BCR/ABL1 or P210 BCR/ABL1 resulted in expansion of erythroid cells and stimulated erythropoietin-independent burst-forming unit-erythroid colony formation. By using a lentiviral anti-signal transducer and activator of transcription 5 (STAT5) short-hairpin RNA, we found that both P190 BCR/ABL1- and P210 BCR/ABL1-induced erythroid cell expansion were STAT5-dependent. Under in vitro conditions favoring B-cell differentiation, neither P190 nor P210 BCR/ABL1-expressing cells formed detectable levels of CD19-positive cells. Gene expression profiling revealed that P190 BCR/ABL1 and P210 BCR/ABL1 induced almost identical gene expression profiles, and we identified a common set of 222 differentially expressed genes. Our data suggest that the early cellular and transcriptional effects of P190 BCR/ABL1 and P210 BCR/ABL1 expression are very similar when they are expressed in the same human progenitor cell population, and that STAT5 is an important regulator of BCR/ABL1-induced erythroid cell expansion. Keywords: global gene expression profiling, BCR/ABL1, CD34+ cord blood cells, CML, Ph+ ALL

2009-05-12 | GSE16042 | GEO

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Project description:Compared with naïve B cells, the B cell receptor (BCR) signal in germinal center (GC) B cells is attenuated; however, the significance of this signaling attenuation has not been well defined. Here, to investigate the role of attenuation of BCR signaling, we employed a Csk mutant mouse model in which Csk-deficiency in GC B cells resulted in augmentation of net BCR signaling with no apparent effect on antigen presentation. We found that Csk is required for GC maintenance and efficient antibody affinity maturation. Mechanistically, ROS-induced apoptosis was exacerbated concomitantly with mitochondrial dysfunction in Csk-deficient GC B cells. Hence, our data suggest that attenuation of the BCR signal restrains hyper-ROS production, thereby protecting GC B cells from apoptosis and contributing to efficient affinity maturation.

2024-05-06 | GSE244802 | GEO

Transcription factor EB sets the stage for fate decisions of antigen-primed B cells in the absence and presence of co-stimulation

Project description:Ligation of the B cell antigen receptor (BCR) initiates humoral immunity. However, mere BCR signaling without appropriate co-stimulation commits B cells to death rather than to differentiation into immune effector cells. How BCR activation depletes potentially autoreactive B cells while simultaneously primes for receiving rescue and differentiation signals from cognate T lymphocytes remains unknown. Here, using a mass spectrometry-based proteomic approach to identify cytosolic/nuclear shuttling elements, we uncover transcription factor EB (TFEB) as a central BCR-controlled rheostat that drives activation-induced apoptosis, and concurrently, promotes the reception of co-stimulatory rescue signals by supporting B cell migration and antigen presentation. CD40 co-stimulation prevents TFEB-driven cell death, while enhancing and prolonging TFEB’s nuclear residency, which hallmarks antigenic experience also of memory B cells. In mice, TFEB shapes the transcriptional landscape of germinal center B cells. Within the germinal center, TFEB facilitates the dark zone entry of light-zone-residing centrocytes through regulation of chemokine receptors and, by balancing the expression of Bcl-2/BH3-only family members, integrates antigen-induced apoptosis with T cell-provided CD40 survival signals. Thus, TFEB reprograms antigen-primed germinal center B cells for cell fate decisions.

2024-08-08 | PXD054505 | Pride

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