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Expression of Human naïve B cell priming for plasma cell differentiation

ABSTRACT: To explore events that govern the differentiation of human naïve B cells (NBCs) into memory B cells and plasma cells (PCs), we designed an in vitro 2-step culture model leading non-switched NBC precursors to differentiate into two cell compartments: CD20loCD38hi and CD20+CD38+. Both populations are characterized by distinct cell fates, the former one corresponding to plasmablasts that undergo PC terminal differentiation, with intermingled relationship between cell division and bona fide differentiation two events that are usually viewed as mutually exclusive. Postulating that extracellular cues mediated by distinct receptor-ligand interactions are likely involved in this phenomenon we explored one by one factors used in our model and found that T-cell-produced IL-2 was critical for the PC’s commitment. Interestingly, this IL-2 effect operates independently of proliferation and survival functions and required an ERK signaling. Based on our study we proposed to complete previous scheme of PRDM1/Blimp-1 controlling PC differentiation by adding the T-cell-delivered IL-2 effect, which sustains indirectly the mitogenic-induced Blimp-1 expression by downregulating IRF8 and BACH2 via an ERK signal This study highlight early events that could take place when cognate B and T cells meet and interact before seeding follicle, where crucial inputs may condition final GC B destiny.

ORGANISM(S): Homo sapiens

PROVIDER: GSE36975 | GEO | 2012/04/09

SECONDARY ACCESSION(S): PRJNA157513

REPOSITORIES: GEO

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Expression of Human naïve B cell priming for plasma cell differentiation

Project description:To explore events that govern the differentiation of human naïve B cells (NBCs) into memory B cells and plasma cells (PCs), we designed an in vitro 2-step culture model leading non-switched NBC precursors to differentiate into two cell compartments: CD20loCD38hi and CD20+CD38+. Both populations are characterized by distinct cell fates, the former one corresponding to plasmablasts that undergo PC terminal differentiation, with intermingled relationship between cell division and bona fide differentiation two events that are usually viewed as mutually exclusive. Postulating that extracellular cues mediated by distinct receptor-ligand interactions are likely involved in this phenomenon we explored one by one factors used in our model and found that T-cell-produced IL-2 was critical for the PC’s commitment. Interestingly, this IL-2 effect operates independently of proliferation and survival functions and required an ERK signaling. Based on our study we proposed to complete previous scheme of PRDM1/Blimp-1 controlling PC differentiation by adding the T-cell-delivered IL-2 effect, which sustains indirectly the mitogenic-induced Blimp-1 expression by downregulating IRF8 and BACH2 via an ERK signal This study highlight early events that could take place when cognate B and T cells meet and interact before seeding follicle, where crucial inputs may condition final GC B destiny. GEP was performed on the RNA of purified B cells from 3 healthy blood donors, stimulated at Day 0 and with addition or not of IL-2. Four time points were assessed Day 0, Day 0+16h, Day 0+22h and Day 4.

2012-04-08 | E-GEOD-36975 | biostudies-arrayexpress

Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

Project description:Gene expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. Patient CLL01 was also treated with IL-4 plus 5 mg/ml ERK activation inhibitor peptide I, or IL-4 plus 10 ÂµM NFkB activation inhibitor, and IL-4 plus 100 mg/ml cyclic-pifithrin-Î± 23 CLL patients (10 Pre samples, 23 Ctrl samples, 23 IL-4 samples, 1 IL-4 plus ERK inhibitor sample, 1 IL-4 plus NFkB inhibitor sample, 1 IL-4 plus Pifithrin sample), 13 NBC (10 Pre samples, 10 Ctrl samples, 13 IL-4 samples)

2014-10-06 | E-GEOD-55288 | biostudies-arrayexpress

Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

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IL-10 induces a STAT3-dependent autoregulatory loop in Th2 cells that promotes Blimp-1 restriction of cell expansion via antagonism of STAT5 target genes

Project description:Blimp-1 expression in T cells extinguishes the T follicular helper cell fate and drives terminal differentiation, but also limits autoimmunity. Although various factors have been described to control Blimp-1 expression in T cells, little is known about what regulates Blimp-1 expression in Th2 cells and the molecular basis of its actions. Herein, we report that STAT3 unexpectedly played a critical role in regulating Blimp-1 in Th2 cells. Furthermore, we found that the cytokine IL-10 acted directly on Th2 cells and was necessary and sufficient to induce optimal Blimp-1 expression through STAT3. Together, Blimp-1 and STAT3 amplified IL-10 production in Th2 cells, creating a strong autoregulatory loop that enhanced Blimp-1 expression. Increased Blimp-1 in T cells antagonized STAT5-regulated cell cycle and anti-apoptotic genes to limit cell expansion. These data elucidate the signals required for Blimp-1 expression in Th2 cells and reveal an unexpected mechanism of action of IL-10 in T cells, providing insights into the molecular underpinning by which Blimp-1 constrains T cell expansion to limit autoimmunity.

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miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

Project description:miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. 16 CLL patients (8 Pre samples, 15 Ctrl samples, 15 IL-4 samples), 3 NBC (3 Ctrl samples, 3 IL-4 samples)

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Spatial microniches of IL-2 synergize with IL-10 to drive lung migratory Th2 cells in response to inhaled allergen [Spatial transcriptomics]

Project description:The mechanisms that guide Th2 cell differentiation in barrier tissues are unclear but important for the development of allergic asthma. Using temporal, spatial and single cell transcriptomic tracking of house dust mite (HDM) specific T cells, we describe the molecular pathways driving allergen-specific Th2 cells. Early Blimp-1 expression occurs in a subset of CD4 T cells in the lymph node prior to lung migration driven by IL-10 from allergen-specific T cells, but was not required for GATA3 upregulation. Instead, IL-2 via STAT5 was required to directly repress Bcl6 and Bach2 to support GATA3 and Blimp-1 upregulation. Loss of Blimp-1 during priming in the lymph node ablated the formation of Th2 cells that migrate to the lung, indicating early Blimp-1 promotes the population of Th2 cells with migratory capability. Spatial microniches of IL-2 in the lymph node discriminate and support these earliest Blimp-1+ migratory Th2 cells, demonstrating that lymph node localization is a primary driver of differentiation. Our findings illuminate the molecular pathways for inhaled allergens to promote Th2 cells and identify an early requirement for IL-2 mediated spatial microniches and allergen-driven IL-10 from responding T cells that drive allergic asthma.

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Spatial microniches of IL-2 synergize with IL-10 to drive lung migratory Th2 cells in response to inhaled allergen [scRNA-Seq]

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Spatial microniches of IL-2 synergize with IL-10 to drive lung migratory Th2 cells in response to inhaled allergen [Curio]

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Transcriptome analysis of early differentiating Tfh vs Th1 cells

Project description:Comparison of transcriptome between early Tfh vs. early Th1 cells Blimp-1-YFP LCMV gp specific TCRtg Smarta cells were transferred into B6 mice, which were then infected with LCMV Armstrong. On day 3 after infection, splenocytes were stained to sort Blimp-1-YFP+IL-2Ra+ Th1 cells or Blimp-1-YFP-IL-2Ra- Tfh cells for RNAseq analysis. Contributor: LIAI RNAi center (LIAI)

2015-07-27 | E-GEOD-67334 | biostudies-arrayexpress

BACH2 in human plasma cell fate decision

Project description:We report here the broad transcriptomic program regulated by BACH2 transcription factor. We used a well suited in vitro model of B cell differentiation to evaluate transcriptomic program governed by BACH2 leading to Plasmocyte (PC) differentiation. In this model B cells were cultured with anti-BCR, CpG, CD40L and Interleukin-2 (IL2). This Interleukin triggers PC differentiation by directly repressing BACH2 expression. We artificially inhibit BACH2 expression by siRNA and found that this condition is sufficient to trigger PC differentiation without IL2. To understand global changes induced by enforced BACH2 downregulation we compared Chip-Sequencing data between activated B Cells and BACH2 deficient B cells (siBACH2). We found that BACH2 binds more than 3000 genes across the human genome. RNAsequencing comparing IL2 drivent committed cells and siBACH2 committed cells highlighs a large common trasncriptional program shared by both conditions and involved in B cell destiny. This study provides evidence that BACH2 is a guardian of B cell fate.

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