RNA-seq analysis of human NK cells expanded with 221-mIL21 expansion system and K562-mIL21 expansion system
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ABSTRACT:
PROVIDER: PRJNA655694 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12401852.fastq.gz | Fastqsanger.gz | |||
| SRR12401853.fastq.gz | Fastqsanger.gz | |||
| SRR12401854.fastq.gz | Fastqsanger.gz | |||
| SRR12401855.fastq.gz | Fastqsanger.gz | |||
| SRR12401856.fastq.gz | Fastqsanger.gz |
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Project description:PBMCs were stimulated with irradiated K562-mIL21 and 221-mIL21 feeder cells, respectively, as well as supplemented with IL-2 and IL-15. NK cells were purified from expanded cells using flow cytometry on day 7 and day 14 for RNA sequencing (RNA-Seq).
2020-08-07 | GSE155812 | GEO
Project description:Natural Killer cells (NK), a major constituent of innate immune system, have the ability to kill the transformed and infected cells without prior sensitization; can be put to immunotherapeutic use against various malignancies. NK cells discriminate between normal cells and transformed cells via a balance of inhibitory and activating signals induced by interactions between NK cell receptors and target cell ligands. Present study investigates whether expansion of NK cells could augment their anti-myeloma (MM) activity. For NK cell expansion, peripheral blood mononuclear cells from healthy donors and myeloma patients were co-cultured with irradiated K562 cells transfected with 4-1BBL and membrane-bound IL15 (K562-mb15-41BBL). A genome-wide profiling approach was performed to identify gene expression signature in expanded NK (ENK) cells and non-expanded NK cells isolated from healthy donors and myeloma patients. A specific set of genes involved in proliferation, migration, adhesion, cytotoxicity, and activation were up regulated post expansion, also confirmed by flow cytometry. Exp-NK cells killed both allogeneic and autologous primary MM cells more avidly than non-exp-NK cells in vitro. Multiple receptors, particularly NKG2D, natural cytotoxicity receptors, and DNAM-1 contributed to target lysis, via a perforin mediated mechanism. In summary, vigorous expansion and high anti-MM activity both in vitro and in vivo provide the rationale for testing exp-NK cells in a clinical trial for high risk MM. Differential gene expression profile in expanded natural killer (ENK) cells and non-expanded natural killer (NK) cells from healthy donors and myeloma patients Eight healthy donor and eight myeloma patients were used in the study. Non-expanded natural killer (NK) cells were isolated from PBMCs of healthy donors and myeloma patients. Expanded natural killer (ENK) cells were generated from same set of samples as mentioned in expansion protocol. All ENK and NK cells were used for gene expression profiling.
2011-03-08 | E-GEOD-27838 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) constitute fine tuners of gene expression and are implicated in a variety of diseases spanning from inflammation to cancer. miRNA expression is deregulated in rheumatoid arthritis (RA), however, their specific role in key arthritogenic cells such as the synovial fibroblast (SF) remains elusive. We have shown in the past that the expression of the miR-221/222 cluster is upregulated in RA SFs. Here, we demonstrate that miR-221/222 activation is downstream of major inflammatory cytokines, such as TNF and IL-1β, which promote miR-221/222 expression independently. miR-221/222 expression in SFs from the huTNFtg mouse model of arthritis correlates with disease progression. Targeted transgenic overexpression of miR-221/222 in SFs of the huTNFtg mouse model led to further expansion of synovial fibroblasts and disease exacerbation. miR-221/222 overexpression altered the transcriptional profile of SFs igniting pathways involved in cell cycle progression and ECM regulation. Validated targets of miR-221/222 included p27 and p57 cell cycle inhibitors, as well as Smarca1 (a chromatin remodeling component). In contrast, complete genetic ablation of miR-221/222 in arthritic mice led to decreased proliferation of fibroblasts, reduced synovial expansion and attenuated disease. scATAC-seq data analysis revealed increased miR-221/222 gene activity in the pathogenic and activated clusters of the intermediate and lining compartment. Taken together, our results establish an SF-specific pathogenic role of the miR-221/222 cluster in arthritis and suggest that its therapeutic targeting in specific subpopulations should inform the design of novel fibroblast-targeted therapies for human disease.
2022-12-16 | GSE210887 | GEO
Project description:Natural Killer cells (NK), a major constituent of innate immune system, have the ability to kill the transformed and infected cells without prior sensitization; can be put to immunotherapeutic use against various malignancies. NK cells discriminate between normal cells and transformed cells via a balance of inhibitory and activating signals induced by interactions between NK cell receptors and target cell ligands. Present study investigates whether expansion of NK cells could augment their anti-myeloma (MM) activity. For NK cell expansion, peripheral blood mononuclear cells from healthy donors and myeloma patients were co-cultured with irradiated K562 cells transfected with 4-1BBL and membrane-bound IL15 (K562-mb15-41BBL). A genome-wide profiling approach was performed to identify gene expression signature in expanded NK (ENK) cells and non-expanded NK cells isolated from healthy donors and myeloma patients. A specific set of genes involved in proliferation, migration, adhesion, cytotoxicity, and activation were up regulated post expansion, also confirmed by flow cytometry. Exp-NK cells killed both allogeneic and autologous primary MM cells more avidly than non-exp-NK cells in vitro. Multiple receptors, particularly NKG2D, natural cytotoxicity receptors, and DNAM-1 contributed to target lysis, via a perforin mediated mechanism. In summary, vigorous expansion and high anti-MM activity both in vitro and in vivo provide the rationale for testing exp-NK cells in a clinical trial for high risk MM. Differential gene expression profile in expanded natural killer (ENK) cells and non-expanded natural killer (NK) cells from healthy donors and myeloma patients
2011-03-08 | GSE27838 | GEO
Project description:K562 and 221 cells
2020-08-07 | GSE155813 | GEO
Project description:miR-221/222 drive synovial fibroblast expansion and pathogenesis of TNF-mediated arthritis
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Project description:Sinorhizobium meliloti 221 Resequencing
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Project description:Expansion of triplex-forming GAA/TTC repeats in the first intron of FRDA gene is known to cause Friedreich’s ataxia. Besides FRDA, there are a number of other highly polymorphic GAA/TTC loci in the human genome where the size variations so far were considered to be a neutral event. Using yeast as a model system, we demonstrate that expanded GAA/TTC repeats represent a threat to eukaryotic genome integrity by triggering double-strand breaks and gross chromosomal rearrangements. The fragility potential strongly depends on the length of the track and orientation of the repeats relative to the replication origin which correlates with their propensity to adopt secondary structure and to block replication progression. We show that fragility is mediated by mismatch repair machinery and requires the MutS(beta) and endonuclease activity of MutL(alpha). We suggest that the mechanism of GAA/TTC-induced chromosome aberrations defined in yeast can also operate in human carriers with expanded tracks. Keywords: CGH-array Genomic DNA from each of 15 strains was competitively hybridized to DNA from the parent diploid strain (Cy3/green). Gains of genomic segments in the survivors were detected as continuous regions of positive Log2 Red:Green ratios, while losses were detected as negative Log2 Red:Green ratios.
2008-05-14 | E-GEOD-11425 | biostudies-arrayexpress
Project description:Expansion of triplex-forming GAA/TTC repeats in the first intron of FRDA gene is known to cause Friedreich’s ataxia. Besides FRDA, there are a number of other highly polymorphic GAA/TTC loci in the human genome where the size variations so far were considered to be a neutral event. Using yeast as a model system, we demonstrate that expanded GAA/TTC repeats represent a threat to eukaryotic genome integrity by triggering double-strand breaks and gross chromosomal rearrangements. The fragility potential strongly depends on the length of the track and orientation of the repeats relative to the replication origin which correlates with their propensity to adopt secondary structure and to block replication progression. We show that fragility is mediated by mismatch repair machinery and requires the MutS(beta) and endonuclease activity of MutL(alpha). We suggest that the mechanism of GAA/TTC-induced chromosome aberrations defined in yeast can also operate in human carriers with expanded tracks. Keywords: CGH-array
2008-05-14 | GSE11425 | GEO