Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA253119 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ZBTB20 is an adjuvant-specific factor for long-term antibody responses. This factor is critical for maintaining long-lived plasma cells in alum-adjuvanted antibody responses but is dispensable for TLR ligand-adjuvanted responses. To identify the functions of ZBTB20 in long-lived plasma cells, we performed microarray analysis on Zbtb20-sufficient and Zbtb20-deficient polyclonal bone marrow plasma cells under the assumption that ZBTB20 regulates relevant targets in all long-lived plasma cells, irrespective of their mode of formation. Chimeras were generated using Zbtb20-sufficient (WT) or Zbtb20-deficient (TRAP) E14.5 fetal livers. 3-4 months after reconstitution, donor bone marrow B220low/-CD138+ cells (4 replicates per genotype) were purified via FACS for microarray. In total, 8 samples, 4 for each genotype, were included in this study.
2014-06-19 | E-GEOD-58659 | biostudies-arrayexpress
Project description:ZBTB20 is an adjuvant-specific factor for long-term antibody responses. This factor is critical for maintaining long-lived plasma cells in alum-adjuvanted antibody responses but is dispensable for TLR ligand-adjuvanted responses. To identify the functions of ZBTB20 in long-lived plasma cells, we performed microarray analysis on Zbtb20-sufficient and Zbtb20-deficient polyclonal bone marrow plasma cells under the assumption that ZBTB20 regulates relevant targets in all long-lived plasma cells, irrespective of their mode of formation.
2014-06-19 | GSE58659 | GEO
Project description:Trancriptional comparison of Zbtb32-deficient and -sufficient polyclonal resting memory B cells
| PRJNA325335 | ENA
Project description:B cells provide humoral immunity by differentiating into antibody-secreting plasma cells, a process that requires cell division and is linked to DNA hypomethylation and gene regulation. Conversely, accumulation of DNA methylation in B cell differentiation is less apparent. To determine the role of de novo DNA methylation in B cell differentiation, the de novo DNA methyltransferases, Dnmt3a and Dnmt3b, were deleted in B cells resulting in phenotypically normal B cell development in the bone marrow, spleen and lymph nodes. However, upon immunologic challenge, mice deficient for Dnmt3a and Dnmt3b (Dnmt3-deficient) accumulated more antigen-specific B cells and bone marrow chimeras showed this was cell-autonomous. Additionally, a five-fold increase in splenic and bone marrow plasma cells was observed. Molecular analysis revealed that Dnmt3-deficient bone marrow plasma cells failed to repress gene expression to the same level as their Dnmt3ab-sufficient counterparts. This was coupled with a failure of Dnmt3-deficient germinal center B cells and plasma cells to gain and/or maintain DNA methylation at several thousand loci that were clustered in enhancers of genes that function in B cell activation and homing. Analysis of chromatin accessibility showed Dnmt3-deficient plasma cells had increased accessibility at several genes involved in hematopoiesis and B cell differentiation. These data show that de novo DNA methylation limits B cell activation, proliferation and differentiation, and support a model whereby DNA methylation represses the aberrant transcription of genes silenced in B cell differentiation to maintain plasma cell homeostasis.
2017-12-31 | GSE89470 | GEO
Project description:B cells provide humoral immunity by differentiating into antibody-secreting plasma cells, a process that requires cell division and is linked to DNA hypomethylation and gene regulation. Conversely, accumulation of DNA methylation in B cell differentiation is less apparent. To determine the role of de novo DNA methylation in B cell differentiation, the de novo DNA methyltransferases, Dnmt3a and Dnmt3b, were deleted in B cells resulting in phenotypically normal B cell development in the bone marrow, spleen and lymph nodes. However, upon immunologic challenge, mice deficient for Dnmt3a and Dnmt3b (Dnmt3-deficient) accumulated more antigen-specific B cells and bone marrow chimeras showed this was cell-autonomous. Additionally, a five-fold increase in splenic and bone marrow plasma cells was observed. Molecular analysis revealed that Dnmt3-deficient bone marrow plasma cells failed to repress gene expression to the same level as their Dnmt3ab-sufficient counterparts. This was coupled with a failure of Dnmt3-deficient germinal center B cells and plasma cells to gain and/or maintain DNA methylation at several thousand loci that were clustered in enhancers of genes that function in B cell activation and homing. Analysis of chromatin accessibility showed Dnmt3-deficient plasma cells had increased accessibility at several genes involved in hematopoiesis and B cell differentiation. These data show that de novo DNA methylation limits B cell activation, proliferation and differentiation, and support a model whereby DNA methylation represses the aberrant transcription of genes silenced in B cell differentiation to maintain plasma cell homeostasis.
2017-12-31 | GSE89467 | GEO
Project description:B cells provide humoral immunity by differentiating into antibody-secreting plasma cells, a process that requires cell division and is linked to DNA hypomethylation and gene regulation. Conversely, accumulation of DNA methylation in B cell differentiation is less apparent. To determine the role of de novo DNA methylation in B cell differentiation, the de novo DNA methyltransferases, Dnmt3a and Dnmt3b, were deleted in B cells resulting in phenotypically normal B cell development in the bone marrow, spleen and lymph nodes. However, upon immunologic challenge, mice deficient for Dnmt3a and Dnmt3b (Dnmt3-deficient) accumulated more antigen-specific B cells and bone marrow chimeras showed this was cell-autonomous. Additionally, a five-fold increase in splenic and bone marrow plasma cells was observed. Molecular analysis revealed that Dnmt3-deficient bone marrow plasma cells failed to repress gene expression to the same level as their Dnmt3ab-sufficient counterparts. This was coupled with a failure of Dnmt3-deficient germinal center B cells and plasma cells to gain and/or maintain DNA methylation at several thousand loci that were clustered in enhancers of genes that function in B cell activation and homing. Analysis of chromatin accessibility showed Dnmt3-deficient plasma cells had increased accessibility at several genes involved in hematopoiesis and B cell differentiation. These data show that de novo DNA methylation limits B cell activation, proliferation and differentiation, and support a model whereby DNA methylation represses the aberrant transcription of genes silenced in B cell differentiation to maintain plasma cell homeostasis.
2017-12-31 | GSE89412 | GEO
Project description:We found that, among newly generated IgG plasma cells, integrin b7hi marks plasma cells prone to home to the bone marrow, whereas integrin b7lo cells remain in secondary lymphoid organs. Moreover, we also found that the differences in KLF2 expression between b7hi and b7lo populations in secondary lymphoid organs is likely to explain that only integrin b7hi plasma cells can egress. Next, to look for the functional target(s) downstream of KLF2 involved in egress of newly generated plasma cells, we carried out RNA-seq analysis of KLF2-sufficient and -deficient splenic plasma cells. Wildtype control splenic plasma cells were further divided into integrin b7hi and b7lo populations. We identified S1pr1 and Itgam as functional targets downstream of KLF2.
2025-02-05 | GSE266441 | GEO
Project description:genome wide methylation data include: MeDIP-seq and MRE-seq in Vitamin D deficient and sufficient bone marrow cells
2023-08-21 | GSE157195 | GEO
Project description:AL amyloidosis is a disorder characterized by expansion of clonal plasma cells in the bone marrow and distant end organ damage mediated by misfolded immunoglobulin free light chains. There are currently limited data regarding the functional characteristics of AL amyloidosis plasma cells and their surrounding bone marrow microenvironment. We performed 5’ single cell RNA sequencing on 9 newly diagnosed, treatment naive AL amyloidosis patients and 8 healthy subjects. We identified generalized suppression of normal bone marrow hematopoiesis with distinct expansion of CD16 monocytes and subsets of CD4+ T cells in AL amyloidosis patients. We detected significant transcriptional changes broadly occurring among immune cells with increased interferon α and γ response and decreased TNF-α signaling. T and B cell receptor profiling revealed no overt clonal expansion of B or T cells in AL amyloidosis patients. However, we noted a disproportionate expansion of a distinct population of non-malignant plasma cells in AL amyloidosis patients. Finally, clonal AL amyloidosis plasma cells were identified based on their unique VDJ rearrangement and they showed increased expression of genes involved in proteostasis and antigen processing when compared to autologous, polyclonal plasma cells. Inter-patient transcriptional heterogeneity was evident, with transcriptional states reflective of common genomic translocations easily identifiable. Overall, this study defines the transcriptional characteristics of AL amyloidosis plasma cells and their surrounding bone marrow microenvironment, identifying transcriptional signatures that serve as candidates in early diagnosis in larger studies, and potential molecular targets for therapy.
2025-03-18 | GSE292189 | GEO
Project description:Gene expression profile of Pafah2-deficient bone marrow derived mast cells (BMMCs) treated with w3 epoxides or GW9662
2017-02-07 | GSE94527 | GEO