Gene expression profiles from human splenic Marginal Zone and Naive (Follicular) B cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE85289 | GEO | 2017/10/14
SECONDARY ACCESSION(S): PRJNA338083
REPOSITORIES: GEO
Similar Datasets
Project description:Gene expression analysis of splenic follicular B cells and marginal zone B cells from B6 and CD19:KLF3 transgenic mice Comparing KLF3-transgenic and non-transgenic follicular B cells by RNA-microarray revealed that KLF3 regulates a subset of genes that was similarly up-/downregulated upon normal MZ B cell differentiation. Indeed, KLF3 expression overcame the lack of MZ B cells caused by different genetic alterations, such as CD19-deficiency or blockade of B-cell activating factor (BAFF)-receptor signaling, indicating that KLF3 may complement alternative NF-κB signaling. Thus, KLF3 is a driving force towards MZ B cell maturation. RNA of splenic follicular B cells and marginal zone B cells were obtained from 4 different mice per group (B6 and CD19:KLF3 mice). 16 samples = 8 individual mice x 2 B cell subsets.
2011-01-29 | E-GEOD-26948 | biostudies-arrayexpress
Project description:Gene expression analysis of splenic follicular B cells and marginal zone B cells from B6 and CD19:KLF3 transgenic mice Comparing KLF3-transgenic and non-transgenic follicular B cells by RNA-microarray revealed that KLF3 regulates a subset of genes that was similarly up-/downregulated upon normal MZ B cell differentiation. Indeed, KLF3 expression overcame the lack of MZ B cells caused by different genetic alterations, such as CD19-deficiency or blockade of B-cell activating factor (BAFF)-receptor signaling, indicating that KLF3 may complement alternative NF-κB signaling. Thus, KLF3 is a driving force towards MZ B cell maturation.
2011-01-29 | GSE26948 | GEO
Project description:Marginal zone (MZ) B cells have innate-like response characteristics due to a unique ability receive and integrate Notch2 signals in the spleen. There is evidence showing MZ B cells receive these signals both in the marginal sinus and the B cell follicle. The relative strength and conservation of these Notch signals is not yet clear. Therefore, we generated mice in which S1pr1 is deleted in mature B cells. These mice have MZ B cells by phenotype but these cells are retained in the follicle and unable to transit to the marginal zone. In this experiment we examined the impact of Notch2 signaling in these cells and cre expressing control animals using in vivo anti-Notch2 antibody blockade followed by RNA-sequencing.
2024-10-18 | GSE274990 | GEO
Project description:Splenocytes were FACS-sorted from Wild-type and Mir146a-/- mice to isolate specific B-cell developmental stages. Utilizing high-throughput sequencing, we comparatively analyzed developmental stage-specific splenic B cell transcriptomes, including Transitional-1 (T1), Transitional-2 (T2), Marginal zone (MZ) and Follicular (FO) in both Wild-type and Mir146a-/- B cells. Two replicates of each developmental stage were submitted for high-throughput sequencing.
2017-01-15 | GSE93252 | GEO
Project description:Lymphoplasmacytic lymphomas and marginal zone lymphomas of nodal, extra-nodal and splenic types account for 10% of non-Hodgkin lymphomas. They are similar at the cell differentiation level, sometimes making difficult to distinguish them from other indolent non-Hodgkin lymphomas. To better characterize their genetic basis, we performed array-based comparative genomic hybridization in 101 marginal zone lymphomas (46 MALT, 35 splenic and 20 nodal marginal zone lymphomas) and 13 lymphoplasmacytic lymphomas. Overall, 90.1% exhibited copy-number abnormalities. Lymphoplasmacytic lymphomas demonstrated the most complex karyotype (median=7 copy-number abnormalities), followed by MALT (4), nodal (3.5) and splenic marginal zone lymphomas (3). A comparative analysis exposed a group of copy-number abnormalities shared by several or all the entities with few disease-specific abnormalities. Gain of chromosomes 3, 12 and 18 and loss of 6q23-q24 (TNFAIP3) were identified in all entities. Losses of 13q14.3 (MIRN15A-MIRN16-1) and 17p13.3-p12 (TP53) were found in lymphoplasmacytic and splenic marginal zone lymphomas; loss of 11q21-q22 (ATM) in nodal, splenic marginal zone and lymphoplasmacytic lymphomas; loss of 7q32.1-q33 in MALT, splenic and lymphoplasmacytic lymphomas. Abnormalities affecting the NF-kB pathway were observed in 70% of MALT and lymphoplasmacytic lymphomas and 30% of splenic and nodal marginal zone lymphomas, suggesting distinct roles of this pathway in the pathogenesis/progression of these subtypes. Elucidation of the genetic alterations contributing to the pathogenesis of these lymphomas may guide to design specific therapeutic approaches.
2012-01-24 | GSE35278 | GEO
Project description:<p>Splenic Marginal Zone Lymphoma (SMZL) is a B-cell malignancy of unknown pathogenesis and thus orphan of targeted therapies. By integrating whole-exome sequencing and copy-number analysis of 8 paired tumor-normal DNAs from patients with SMZL, we show that the typical SMZL exome carries ~30 genetic alterations. Targeted resequencing of selected candidates in an extended panel of 40-117 samples revealed activating mutations of NOTCH2, a gene required for marginal-zone (MZ) development, as the most frequent and SMZL-specific lesion, accounting for approximately 20% of cases. Additional altered genes suggest that deregulation of signaling pathways normally involved in MZ development (NOTCH, NF-kappa B, and B-cell receptor) represents a critical event in SMZL pathogenesis. These findings have direct implications for the treatment of SMZL patients since drugs are available which can target NOTCH as well as other pathways deregulated in this disease.</p>
| phs000502 | dbGaP
Project description:Lymphoplasmacytic lymphomas and marginal zone lymphomas of nodal, extra-nodal and splenic types account for 10% of non-Hodgkin lymphomas. They are similar at the cell differentiation level, sometimes making difficult to distinguish them from other indolent non-Hodgkin lymphomas. To better characterize their genetic basis, we performed array-based comparative genomic hybridization in 101 marginal zone lymphomas (46 MALT, 35 splenic and 20 nodal marginal zone lymphomas) and 13 lymphoplasmacytic lymphomas. Overall, 90.1% exhibited copy-number abnormalities. Lymphoplasmacytic lymphomas demonstrated the most complex karyotype (median=7 copy-number abnormalities), followed by MALT (4), nodal (3.5) and splenic marginal zone lymphomas (3). A comparative analysis exposed a group of copy-number abnormalities shared by several or all the entities with few disease-specific abnormalities. Gain of chromosomes 3, 12 and 18 and loss of 6q23-q24 (TNFAIP3) were identified in all entities. Losses of 13q14.3 (MIRN15A-MIRN16-1) and 17p13.3-p12 (TP53) were found in lymphoplasmacytic and splenic marginal zone lymphomas; loss of 11q21-q22 (ATM) in nodal, splenic marginal zone and lymphoplasmacytic lymphomas; loss of 7q32.1-q33 in MALT, splenic and lymphoplasmacytic lymphomas. Abnormalities affecting the NF-kB pathway were observed in 70% of MALT and lymphoplasmacytic lymphomas and 30% of splenic and nodal marginal zone lymphomas, suggesting distinct roles of this pathway in the pathogenesis/progression of these subtypes. Elucidation of the genetic alterations contributing to the pathogenesis of these lymphomas may guide to design specific therapeutic approaches. One hundred fourteen patients were included in this study: 46 MALT lymphomas (22 pulmonary, 11 salivary glands, 7 lacrimal glands and 6 gastrointestinal), 35 splenic marginal zone lymphomas, 20 nodal marginal zone lymphomas and 13 non-Waldenström’s Macroglobulinemia lymphoplasmacytic lymphomas. All cases were reviewed prior to study on paraffin sections with immunohistochemistry. Sections of each frozen tissue used for study were also reviewed by histological examination and immunohistochemistry before was submitted for the study.
2012-01-24 | E-GEOD-35278 | biostudies-arrayexpress
Project description:Nodal marginal zone lymphoma (NMZL) is a small B cell neoplasm whose molecular pathogenesis is still essentially unknown and whose differentiation from other small B cell lymphomas is hampered by the lack of specific markers. We have analyzed gene expression, miRNA profile and copy number data from 15 NMZL cases. For comparison, 16 follicular lymphomas, 9 extranodal marginal zone lymphomas, 8 reactive lymph nodes and B-cell subtypes were included. The results were validated by qRT-PCR in an independent series including 61 paraffin-embedded NMZLs. NMZL signature showed an enriched expression of gene sets identifying interleukins, integrins, CD40, PI3K, NF-kB and TGF-Beta; and included genes expressed by normal marginal zone cells and memory B cells. The most highly overexpressed genes were SYK, TACI, CD74, CD82 and CDC42EP5. Genes linked to G2/M and germinal center were downregulated. Comparison of the gene expression profiles of NMZL and FL showed enriched expression of CHIT1, TGFB1 and TACI in NMZL, and BCL6, LMO2 and CD10 in FL. NMZL displayed increased expression of miR-221, miR-223 and let-7f, while FL strongly expressed miR-494. Our study identifies new candidate diagnostic molecules for NMZL and reveals survival pathways activated in NMZL. We have analyzed gene expression, miRNA profile and copy number data from 15 NMZL cases. For comparison, 16 follicular lymphomas, 9 extranodal marginal zone lymphomas, 8 reactive lymph nodes and B-cell subtypes were included. The results were validated by qRT-PCR in an independent series including 61 paraffin-embedded NMZLs
2011-09-20 | E-GEOD-32231 | biostudies-arrayexpress
Project description:Array-based comparative genomic hybridization comparing splenic marginal zone lymphoma (SMZL) specimens with control DNA
2014-01-01 | GSE34768 | GEO
Project description:Immature B cells in spleens of mouse and human differentiate into at least two subsets of mature B cells, the follicular (FO) B cells and the marginal zone (MZ) B cells, but functions, maturation and other properties of these cells are largely unknown. To solve these questions, in this study, we performed transcriptome analyses of FO and MZ B cells sorted from spleens of normal unimmunized mice using gene chips. By comparison of gene expression profiles between FO and MZ B cells, we identified 1226 genes that are expressed higher in FO B cells than in MZ B cells. On the other hand, 1734 genes were found to be expressed higher in MZ B cells than in FO B cells. We noticed that some of differentially expressed genes have been reportedly characterized in FO and MZ B cells, suggesting the reliability of the analysis. By using FACS analyses, we confirmed that CD36, CD68, and CD49e are expressed on MZ B-cells but not on FO B-cells. These results revealed new phenotypic and functional properties of FO and MZ B cells, and set a molecular basis for further studying differentiation and functions of these mature B cells. Experiment Overall Design: one follicular B cells replicate and one marginal zone B cells replicate were analyzed.
2008-06-12 | E-GEOD-3599 | biostudies-arrayexpress