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Plasma cell mitochondrial pyruvate import controls the duration of humoral immunity.

ABSTRACT: RNA-sequencing was performed on human CD19- CD138+ bone marrow plasma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE81443 | GEO | 2016/05/14

SECONDARY ACCESSION(S): PRJNA321547

REPOSITORIES: GEO

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Plasma cell mitochondrial pyruvate import controls the duration of humoral immunity.

Project description:RNA-sequencing was performed on human CD19- CD138+ bone marrow plasma cells. 4 biological replicates of human CD19- CD138+ bone marrow plasma cells.

2016-05-14 | E-GEOD-81443 | biostudies-arrayexpress

Transcriptome analysis of human colonic IgA+ plasma cell subsets and naïve B cells

Project description:Immunoglobulin A (IgA) is the most abundant antibody in the intestinal tract. Recent studies show that discrete subsets of gut human plasma cells (PCs) release IgA, which contributes to the maintenance of gut homeostasis. To better characterize the properties of these PC subsets, we performed global transcriptome analysis in naïve B cells as well as immature CD19+IgA+CD138- PCs, mature CD19+IgA+CD138+ PCs and late CD19-IgA+CD138+ PCs after their purification from human colon samples.

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Mitochondrial Pyruvate Import Promotes Long-Term Survival of Antibody-Secreting Plasma Cells.

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Gene expression in primary human bone marrow plasma cells sorted according to CD19 expression

Project description:To characterize human bone marrow plasma cells that express or lack CD19 on a molecular level, we compared the global gene expression of primary CD38high/CD138+ plasma cells with or without CD19 expression.

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Transcription profiling of human Waldenstroms macroglobulinemia CD19+ WM B cells (WM-BC) and CD138+ WM plasma cells (WM-PC) with those of normal CD19+ peripheral blood B cells (PB-BC), tonsil-BC (T-BC), CD138+ T-PC and bone marrow PC (N-PC) reveals biological insights into its pathophysiology

Project description:Waldenströms macroglobulinemia (WM) is a rare lymphoproliferative disorder with apparent morphologic and immunophenotypic heterogeneity and its origins are still poorly understood. In this study, using Gene-Expression Profiling (GEP), we compared the global mRNA expression patterns of CD19+ WM B cells (WM-BC) and CD138+ WM plasma cells (WM-PC) with those of normal CD19+ peripheral blood B cells (PB-BC), tonsil-BC (T-BC), CD138+ T-PC and bone marrow PC (N-PC). Experiment Overall Design: The sample cohort studied consisted of CD19-selected peripheral blood B cells (PB-BC; n = 7), tonsil B cells (T-BC; n = 7), bone marrow B cells from WM (WM-BC; n = 12), tonsil plasma cells (T-PC; n = 9), bone marrow plasma cells from healthy donors (N-PC; n = 10), WM plasma cells (WM-PC, n = 9), and MM plasma cells (MM-PC; n = 11).

2008-12-05 | E-GEOD-9656 | biostudies-arrayexpress

CHK1 dosage in germinal center B cells controls humoral immunity.

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Mitochondrial pyruvate import is a metabolic vulnerability in androgen receptor-driven prostate cancer.

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Gene Expression Profiling Reveals Biological Insights into the Pathophysiology of Waldenströms macroglobulinemia

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GLUT1-mediated glucose import in B cells is critical for anaplerotic balance and humoral immunity

Project description:Glucose uptake increases during B cell activation and plasma cell differentiation. However, conflicting findings regarding the role of glucose at different stages of B cell activation prevents establishing a clear metabolic profile. To determine whether glucose is required for establishing humoral immunity, we deleted the glucose transporter type 1 (GLUT1)-encoding gene (Slc2a1fl/fl) in mature B cells by CD23-mediated Cre expression (GLUT1-cKO). While B cell development was normal, germinal center B cell and antibody-secreting cell numbers (ASCs) were severely reduced in GLUT1-cKO mice. In addition, these mice could hardly mount antigen-specific antibody titers after vaccination. Activation of GLUT1-deficient B cells in vitro was impaired and the remaining plasmablasts abolished glycolysis, relying on mitochondrial activity and fatty acid metabolism. Metabolomics combined with genome-wide transcriptome analysis revealed a dramatically altered anaplerotic balance in GLUT1-deficient ASCs. Although the cells attempt to compensate for glucose deprivation by increasing their mitochondrial mass and the expression of genes responsible for glycolysis, the tricarboxylic acid cycle and the hexosamine synthesis pathways, they lack both the necessary metabolites for energy production and functional mitochondrial respiration. Consequently, protein synthesis was limited in GLUT1-deficient ASCs. Thus, we identified GLUT1 as a critical metabolic player defining the germinal center response and humoral immunity.

2024-02-09 | GSE230073 | GEO

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