Comparative analysis of B cell receptor repertoires revealed a delay in CD24hiCD38hi transitional B lymphocyte maturation in Multiple Sclerosis patients
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina MiSeq
ORGANISM(S): Homo sapiens
SUBMITTER: Ivan Zvyagin
PROVIDER: E-MTAB-10859 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To date nothing is known about the specificity of regulatory B cells. Here we analyzed the B cell repertoire at the Ig gene level of regulatory transitional CD24(high)CD38(high) B cells of patients with multiple sclerosis (MS) in comparison with healthy donors. 5 patients with highly active MS, 4 patients with benign MS and 6 healthy donors were examined. Mononuclear cells from peripheral blood were stained against CD19, CD24 and CD38 surface markers. Subpopulation CD19(+)CD24(high)CD38(high) and total pool of CD19(+) cells were sorted individually for subsequent RNA isolation and BCR sequences comparison. Variable heavy (VH) and light (VL) chains genes of each patient were amplified from cDNA and deep sequencing of the VH and VL genes was carried out.
2020-09-24 | E-MTAB-9573 | biostudies-arrayexpress
Project description:In response to antigen challenge, human B cells clonally expand, undergo selection and differentiate within secondary lymphoid tissues to produce mature B cell subsets and high affinity antibodies necessary for an effective immune response. However, the interplay between affinity, antibody class and different B cell fates has proved challenging to decipher in primary human tissue. We have applied an integrated analysis of bulk and single-cell antibody repertoires paired with single-cell transcriptomics of human B cells from a model secondary lymphoid tissue. Specifically, here we have performed bulk B cell repertoire sequencing of the immunoglobulin heavy chain (IgH) for sorted B cell subsets from paediatric tonsil tissue. Matched single-cell gene expression and single-cell VDJ data are also available for the same patient donors.
2020-05-01 | E-MTAB-8999 | biostudies-arrayexpress
Project description:In this study monoclonal cell lines carrying mutations in IFITM3 gene were obtained based on WI-38 VA13 cells. To research the involvement of the IFITM3 gene in cellular response to Influenza A virus infection, original WI-38 VA13 cells and the clones with depressed IFITM3 gene activity (F3, F5, Е12) were infected with influenza A/Puerto Rico/8/1934 (H1N1) virus. RNA-seq analysis of infected cell lines after 24 h was performed on an Illumina NextSeq 500 platform. The same mock-infected cells were used as controls (0 hpi). PolyA RNA-enriched fraction was used for constructing of cDNA libraries. Differential expressed genes were identified using R package DESeq2.
2023-12-16 | E-MTAB-13582 | biostudies-arrayexpress
Project description:To study genes involved in cellular response to Influenza A virus infection, human cells MRC5, WI-38 VA-13, A549 and HEK293FT were infected with influenza A/Puerto Rico/8/1934 (H1N1) virus. RNA-seq analysis of infected cell lines after 48 h was performed on an Illumina NextSeq 500 platform. The same mock-infected cells were used as controls. PolyA RNA-enriched fraction was used for constructing of cDNA libraries. Differential expressed genes were identified using R package DESeq2.
2020-11-23 | E-MTAB-9511 | biostudies-arrayexpress
Project description:To study expression pattern of small nucleolar RNAs (snoRNAs) during influenza A viral infection, human cells A549 were infected with influenza A/Puerto Rico/8/1934 (H1N1) virus. Small RNA-seq analysis of infected cells after 24 h or 48 h incubation was performed on an Illumina NextSeq 500 platform. The same mock-infected cells were used as control. Small RNA fractions (<200 nucleotide length) was used for constructing of cDNA libraries. Differential expressed non-coding RNAs were identified using R package DESeq2.
2022-11-01 | E-MTAB-12088 | biostudies-arrayexpress
Project description:Mechanisms regulating gene expression in malaria parasites are not well understood. Little is known about how this parasite regulates its gene expression during transition from one developmental stage to another and in response to various environmental conditions. Parasites in a diseased host face environments which differ from the static, well adapted in vitro conditions in culture. Parasites thus need to adapt quickly and effectively to these conditions by establishing transcriptional states which is best suited for better survival. With the discovery of natural antisense transcripts (NATs) in this parasite and considering the various proposed mechanisms by which NATs might regulate gene expression, it has been speculated that these might be playing a critical role in gene regulation. We report here the diversity of NATs that exist in this parasite, using isolates taken directly from patients with differing clinical symptoms caused by malaria infection. A total of 797 NATs targeted against annotated loci have been detected using a custom designed strand specific microarray. Out of these, 545 are unique to this study. The majority of NATs were positively correlated with the expression pattern of the sense transcript. Many were found to be differentially regulated in response to disease conditions. Antisense transcripts mapped to a wide variety of biochemical/ metabolic pathways, especially pathways pertaining to the central carbon metabolism and stress related pathways. Our data strongly suggests that a large group of NATs detected here are unannotated transcription units antisense to annotated gene models. The results reveal a previously unknown set of NATs that prevails in this parasite, their differential regulation in disease conditions and mapping to functionally well annotated genes. The results detailed here call for studies to deduce the possible mechanism of action, which would help in understanding the in vivo pathological adaptations of these parasites. Plasmodium falciparum isolates were collected from patients (n = 11) with differing clinical conditions.The patients exhibited symptoms categorized as un-complicated (n =2) or complicated malaria (n = 9). Criteria for determination of complicated disease were based on World Health Organization year 2000 guidelines. Microarray array based transcriptional profiling was carried out to detect prevalence of natural antisense transcript.
2014-04-30 | E-GEOD-44921 | biostudies-arrayexpress
Project description:The toxicity of NBP and its four major metabolites were compared in both PHHs and PRHs, and 3-OH-NBP was found to be the most toxic metabolite. 3-OH-NBP induced remarkable cell death and oxidative stresses in hepatocytes, which correlated well with the levels of glutathione and N-acetylcysteine adducts (3-GSH-NBP and 3-NAC-NBP) in cell supernatants. Additionally, 3-OH-NBP covalently conjugated with intracellular Cys, Lys and Ser, with preferable binding to Cys sites at Myh9 Cys1380, Prdx4 Cys53, Vdac2 Cys48 and Vdac3 Cys36. Furthermore, we found that CYP3A4 induction by rifampicin augmented NBP-induced cell toxicity and supplementing with GSH or NAC alleviated the oxidative stresses and reactive metabolites caused by 3-OH-NBP.
2022-10-22 | PXD029480 | Pride
Project description:The S. cerevisiae Forkhead Box (FOX) proteins, Fkh1 and Fkh2, regulate diverse cellular processes including transcription, long-range DNA interactions during homologous recombination, and replication origin timing and long-range origin clustering. As stimulators of early origin activation, we hypothesized that Fkh1 and Fkh2 abundance limits the rate of origin activation genome-wide. Existing methods, however, were not well suited to quantitative, genome-wide measurements of origin firing between strains and conditions. To overcome this limitation, we developed qBrdU-seq, a quantitative method for BrdU incorporation analysis of replication dynamics, and applied it to show that overexpression of Fkh1 and Fkh2 advance the initiation timing of many origins throughout the genome resulting in a higher total level of origin initiations in early S phase. The higher initiation rate is accompanied by slower replication fork progression, thereby maintaining a normal length of S phase without causing detectable Rad53 checkpoint kinase activation. The advancement of origin firing time, including that of origins in heterochromatic domains, was established in late G1 phase, indicating that origin timing can be reset subsequently to origin licensing. These results provide novel insights into the mechanisms of origin timing regulation by identifying Fkh1 and Fkh2 as rate-limiting factors for origin firing that determine the ability of replication origins to accrue limiting factors and have the potential to reprogram replication timing late in G1 phase. 5 total experiments with replicates
2015-12-18 | E-GEOD-71050 | biostudies-arrayexpress
Project description:We experimentally generated a genome-wide gene expression data. To this end, we first collected samples of three important haploid developmental stages, specifically germinating spores (gametophyte_1), protonemata (gametophyte_2) and young gametophores (gametophyte_3) (four biological replicates each). We also collected three developmental stages of the diploid phase (sporophyte), specifically sporophytes shorter than 5mm (sporophyte_1), elongated needle-like sporophytes (sporophyte_2), and sporophytes with swollen capsules (sporophyte_3)
2013-07-17 | E-MTAB-1664 | biostudies-arrayexpress
Project description:Transcriptome analysis of somatic stem cells and their progeny is fundamental to identify new factors controlling proliferation versus differentiation during tissue formation. Here we generated a combinatorial, fluorescent reporter mouse line to isolate proliferating neural stem cells, differentiating progenitors and newborn neurons that coexist as intermingled cell populations during brain development. Transcriptome sequencing revealed numerous novel long non-coding (lnc)RNAs and uncharacterized protein-coding transcripts identifying the signature of neurogenic commitment. Importantly, most lncRNAs overlapped neurogenic genes and shared with them a nearly identical expression pattern suggesting that lncRNAs control corticogenesis by tuning the expression of nearby cell fate determinants. We assessed the power of our approach by manipulating lncRNAs and protein-coding transcripts with no function in corticogenesis reported to date. This led to several evident phenotypes in neurogenic commitment and neuronal survival indicating that our study provides a remarkably high number of uncharacterized transcripts with hitherto unsuspected roles in brain development. Finally, we focussed on one lncRNA, Miat, whose manipulation was found to trigger pleiotropic effects on brain development and aberrant splicing of Wnt7b. Hence, our study suggests that lncRNA-mediated alternative splicing of cell fate determinants controls stem cell commitment during neurogenesis. M-bM-^@M-^\LncRNAs control neurogenesisM-bM-^@M-^] Aprea, Prenninger, Dori, Monasor, Wessendof, Zocher, Massalini, Ghosh, Alexopoulou, Lesche, Dahl, Groszer, Hiller, Calegari, The EMBO Journal (In Press) mRNA profiles of Proliferating Progenitors, Differentiating Progenitors and Neurons from lateral cortex of E14.5 mouse embryos. Each cell type in three biological replicates.
2013-11-18 | E-GEOD-51606 | biostudies-arrayexpress