Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IKAROS facilitates antigen escape in the face of CD19- and CD22-targeted therapies for B-cell malignancies

ABSTRACT: IKAROS facilitates antigen escape in the face of CD19- and CD22-targeted therapies for B-cell malignancies

PROVIDER: PRJNA937281 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23575200_1.fastq.gz	Fastqsanger.gz
	SRR23575200_2.fastq.gz	Fastqsanger.gz
	SRR23575201_1.fastq.gz	Fastqsanger.gz
	SRR23575201_2.fastq.gz	Fastqsanger.gz
	SRR23575202_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

IKAROS facilitates antigen escape in the face of CD19- and CD22-targeted therapies for B-cell malignancies

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-03-26 | GSE225755 | GEO

Immunotherapy-resistant acute lymphoblastic leukemia cells exhibit reduced CD19 and CD22 expression and BTK pathway dependency [RNA-seq]

Project description:While therapies targeting CD19 by antibodies, CAR-T cells and T cell engagers have improved the response rates in B-cell malignancies; the emergence of resistant cell populations with low CD19 expression can lead to relapsed disease. We developed an in vitro model of adaptive resistance facilitated by chronic exposure of leukemia cells to a CD19-immunotoxin. Single-cell (sc) RNAseq showed increase in transcriptionally distinct CD19low populations in resistant cells. Mass cytometry demonstrated that CD22 was also decreased in these CD19low resistant cells. ATAC-seq showed decreased chromatin accessibility at promoters of both CD19 and CD22 in the resistant cell populations. Combined loss of both CD19 and CD22 antigens was validated in samples from pediatric and young adult patients with B-ALL that relapsed after CD19 CAR-T targeted therapy. Functionally, resistant cells were characterized by slower growth and lower basal levels of MEK activation. CD19low resistant cells exhibited preserved B cell receptor signaling and were more sensitive to both BTK and MEK inhibition. These data demonstrate that resistance to CD19 immunotherapies can result in decreased expression of both CD19 and CD22 and can result in dependency on BTK pathways.

2024-03-06 | GSE255306 | GEO

Immunotherapy-resistant acute lymphoblastic leukemia cells exhibit reduced CD19 and CD22 expression and BTK pathway dependency [ATAC-seq]

2024-03-06 | GSE255305 | GEO

IKAROS modulates CD19 surface expression and CD19-directed CAR-T response [ATAC-seq]

Project description:To elucidate how IKAROS modulates CD19 surface expression in B cell acute lymphoblastic leukemic cells, we analyzed chromatin landscape profile from isogenic IKAROS wild type (WT) or knock down (KD) B-ALL cell lines.

2025-03-27 | GSE225752 | GEO

IKAROS modulates CD19 surface expression and CD19-directed CAR-T response [RNA-seq]

Project description:To elucidate how IKAROS modulates CD19 surface expression in B cell acute lymphoblastic leukemic cells, we analyzed gene expression profile from isogenic IKAROS wild type (WT) or knock down (KD) B-ALL cell lines.

2025-03-27 | GSE225754 | GEO

IKAROS modulates CD19 surface expression and CD19-directed CAR-T response [ATAC-seq]

Project description:IKAROS modulates CD19 surface expression and CD19-directed CAR-T response [ATAC-seq]

| PRJNA937280 | ENA

IKAROS modulates CD19 surface expression and CD19-directed CAR-T response [RNA-seq]

Project description:IKAROS modulates CD19 surface expression and CD19-directed CAR-T response [RNA-seq]

| PRJNA937285 | ENA

CD22 interactome

Project description:CD22 (Siglec-2) is a member of the Siglec family. It is an inhibitory co-receptor of the B-cell-receptor (BCR) and inhibits B–cell activation. Upon BCR stimulation ITIMs in the cytoplasmic tail of CD22 are phosphorylated. This triggers CD22 signalling pathways, which lead to a decreased calcium mobilization in the B cell and thus an inhibition of BCR signalling. Although some CD22 binding partners, such as the phosphatase SHP-1, have already been identified, we deciphered the CD22 interactome in more detail, to gain a deeper understanding of CD22 molecular mechanisms and signalling events after BCR activation. Stable isotope labelling of amino acids in cell culture (SILAC) in combination with mass spectrometry analysis enabled the identification of specific CD22 interaction partners in a quantitative proteomics approach. Hereby, several new CD22 associated proteins were identified that have not been linked to CD22 yet. One of those interacting proteins is cullin 3, an E3 ubiquitin ligase. It was revealed that cullin 3 is important for clathrin-dependent CD22 internalization after BCR stimulation and CD22 surface expression. Further analysis of B-cell specific cullin 3 deficient mice showed an important role of cullin 3 in B cell development. These mice have strongly reduced numbers of mature B cells in the periphery, which are characterized by increased CD22 expression and additionally by pre-activated and apoptotic phenotypes.

2020-05-06 | PXD013801 | Pride

CD22 modulation regulates neuroinflammation in microglia

Project description:Expression data comparing the effect of soluble CD22 in monocyte-derived microlgia and in mouse. Expression data on the effect of SM03 in Aβ-injected AD model in human CD22 transgenic mice.

2024-06-10 | GSE269121 | GEO

Transcriptional responses of T cells activated via CD22-specific T cell receptor compared to CD22-specific chimeric antigen receptor

Project description:Chimeric antigen receptor (CAR) T cells are effective against B-cell malignancies but are associated with cytokine-driven inflammatory toxicities such as cytokine release syndrome (CRS). Historically, T cell receptor (TCR) engineered T cell therapies are rarely associated with CRS. However, it is challenging to compare diverse cell products utilized in different clinical contexts and against different antigens. In this study, TCR and CAR were made to target the same source of antigen, CD22, expressed by B-cell malignancies: the TCR recognizes CD22-derived peptide processed and presented in the context of HLA-A*02:01, and the CAR recognizes CD22 protein expressed on the cell surface. In vivo studies comparing the CD22 TCR-T cells to CD22 CAR-T cells demonstrated that the TCR-T cells could clear leukemia without inducing systemic proinflammatory cytokine elevation, whereas CD22 CAR-T cells induced high levels of circulating proinflammatory cytokine reminiscent of CRS. T cells activated through either the TCR or CAR by an identical leukemia cell line demonstrated differential transcriptional responses. T cells activated via the CAR had disproportionate and significant upregulation of inflammatory gene sets compared to T-cells activated via the TCR.

2025-04-16 | GSE255323 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data